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PPARG activates cell differentiation. 1000 / 1182
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"Because PPARgamma cleavage strongly correlated with metabolic changes in TAMs and the cleavage of PPARgamma impairs its transcriptional activity, we sought to determine whether PPARgamma depletion would promote TAM differentiation and recapitulate the metabolic reprogramming observed in differentiating TAMs."
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"Interestingly, PPARgamma has been reported to crosstalk with activin A : on the one hand, activin A treatment can inhibit PPARgamma expression in 3T3-L1 preadipocytes, leading to reduced adipocytes differentiation [XREF_BIBR]; on the other hand, PPARgamma activation by rosiglitazone can decrease follistatin (activin A antagonist) mRNA levels in rat intestinal epithelial cells, leading to the gain-of-function of activin A, which mediates the effects of TZDs on cell proliferation [XREF_BIBR]."
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"As a gain of function model for mTORC1, this study with TSC1/2 deficient MEFs and 3T3-L1 preadipocytes provides critical support to previous studies suggesting involvement of mTOR signaling in PPARgamma driven adipocyte differentiation, which used rapamycin alone to establish this link XREF_BIBR - XREF_BIBR."
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"Activation of PPARgamma via exogenous ligands such as rosiglitazone or TBT strongly promotes adipocyte differentiation and maintenance, together with the expression of genes involved in lipid droplet formation, glucose uptake, fatty acid synthesis, and adipokine secretion [XREF_BIBR] [XREF_BIBR]."
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"PI3K inhibitor LY294002 did not affect the expression of C/EBPalpha and PPARgamma in un induced 3T3-L1 preadipocytes (P> 0.05), but decreased the expression of C/EBPalpha and PPARgamma during the in vitro induced differentiation of 3T3-L1 preadipocytes compared with the control group (P < 0.05 or 0.01)."
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"We also determined protein levels of two key genes linked to cell proliferation : cyclin D1 which is downstream of multiple pathways leading to increased cell proliferation, and peroxisome proliferation activated receptor gamma (PPARgamma) which inhibits cell proliferation and induces differentiation."
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"Here we show that regulation of the transcriptional coactivator MKL1 (megakaryoblastic leukemia 1) by actin cytoskeleton dynamics drives adipocyte differentiation mediated by peroxisome proliferator activated receptor gamma (PPARgamma), a master transcriptional regulator of adipogenesis."
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"In the development and progression of pancreatic cancer, the activated PPARgamma inhibits tumor cell proliferation and growth and promotes tumor cell apoptosis by inducing cell differentiation, regulating cell cycle and mediating the expression of target genes including apoptotic genes and proapoptotic genes."
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"Attention is given to PPAR-gamma, which in isolation can initiate adipogenic differentiation without inducers, and C/EBPalpha, a second transcription factor induced during adipocyte differentiation, that cooperates with PPAR-gamma to dramatically stimulate the adipocyte program XREF_BIBR."
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"Human breast cancer cells express PPARgamma [XREF_BIBR] and can be targeted, for example, with TZD, and a range of other PPARgamma ligands to induce differentiation and inhibition of cell growth both in vitro and in xenograft models, effects which can be enhanced by cotreatment with either retinoids, TGFbeta or TNFalpha [XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR - XREF_BIBR]."
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"Persistent complete remission of LC upon biomodulatory therapy alone is therefore very noteworthy.Combined transcriptional targeting of peroxisome-proliferator-activated-receptor gamma (PPARγ) and the retinoic acid receptor (RAR) as well as treatment with azacitidine have been previously shown to induce myeloid differentiation and inhibit leukemic cell growth (Curik et al., 2012; Tabe et al., 2012; Faber et al., 2013)."
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"Our study suggested that EWH could promote adipocyte differentiation as shown by increased lipid accumulation, increased release of adiponectin and upregulation of peroxisome proliferator associated receptor gamma (PPARgamma) and CCAAT / enhancer binding protein alpha (C/EBP-alpha)."
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"These researchers demonstrated that PPARgamma activation upregulated osteoclast differentiation by inducing GATA2, which is required to generate osteoclast progenitors, and by activating PPARgamma ligand via c-fos induction, thereby stimulating osteoclast differentiation XREF_BIBR, XREF_BIBR."
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"Also, PPAR-gamma activation by the oxidized lipid fraction leads to differentiation into macrophages where oxLDL stimulated macrophages are prone to migrate through a mechanism dependent on intracellular nitrosative stress and lipid peroxidation favoring their accumulation in the plaque [XREF_BIBR, XREF_BIBR]."
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"In the adipose tissue of these models, expression of adiponectin and peroxisome proliferator activated receptor-gamma (PPARgamma), which induce adipocyte differentiation, and expression of transcription factors of adipocyte differentiation, such as CCAAT-enhancer-binding protein-alpha (C/EBPalpha) and aP2, were decreased."
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"An increase in CiC mRNA abundance and protein level was observed during the induction of murine 3T3-L1 cell differentiation into mature adipocytes, as well as in cells treated with rosiglitazone, a PPARgamma agonist, suggesting the involvement of CiC in adipogenesis [XREF_BIBR, XREF_BIBR]."
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"Activity of the RUNX-2 transcription factor is not only essential for maintenance of osteoblast phenotype, but it is also involved in driving the differentiation of osteoblasts from mesenchymal stem cells [XREF_BIBR - XREF_BIBR], while activity of PPARgamma in mesenchymal stem cells induces differentiation into adipocytes."
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"Other research groups extended these findings by showing that such PPARgamma agonist induced differentiation of A549 and NCI-H23 NSCLC cells reflects sustained extracellular signal regulated kinase 1/2 (ERK1/2) activation that has been linked to cellular differentiation [XREF_BIBR, XREF_BIBR]."
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"In conclusion, we propose that delivery of PPARgamma from microparticles initiates monocyte adherence and possibly differentiation towards a macrophage or " myeloid-endothelial " cell phenotype, but one which is less responsive to inflammatory stimuli than those receiving control microparticles."
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"Further analysis confirmed that CBMG suppressed both the expression and activity of PPARgamma, a master regulator of adipogenesis, and subsequently led to decreases in transcription of C/EBPalpha, aP2, and adiponectin in adipogenesis, thereby attenuating adipocyte differentiation."
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"Our data showed that knockdown of PPARgamma inhibited cells from undergoing efficient neuron differentiation and arrested them at the MSC stage (XREF_FIG) and that physiological concentrations of the PPARgamma agonist rosiglitazone and ectopic expression of PPARgamma accelerated neuron differentiation of hMSCs in vitro (XREF_FIG)."
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"Of note, a peroxisome proliferator activated receptor gamma (PPARgamma) agonist, which did not alter RNAi induced STAT3 inactivation eliminates the suppression of preadipocyte differentiation mediated by inhibition of STAT3, suggesting that STAT3 regulation of adipogenesis occurs upstream of PPARgamma activation [XREF_BIBR]."
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"PPARgamma activated in adipocytes may induce the apoptosis of large fat cells in subcutaneous and visceral deposits in a mouse model and causes the differentiation of preadipocytes into mature fat cells in subcutaneous fat deposit in humans, as well as the up-regulation of pivotal genes associated with triglyceride storage and lipogenesis [XREF_BIBR]."
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"In conclusion, lico E increases the levels of PPARgamma expression, at least in part, via the stimulation of Akt signals and functions as a PPARgamma partial agonist, and this increased PPARgamma expression enhances adipocyte differentiation and increases the population of small adipocytes, resulting in improvements in hyperglycemia and hyperlipidemia under diabetic conditions."
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"We have previously dissected the global transcriptional response of defined immuno selected Lin (Ter119/CD31/CD45) - Sca1 + adipocyte progenitors to carbaprostacyclin (cPGI 2), the stable analogue of prostacyclin and PPARg agonist promoting beige adipocyte differentiation (Vegiopoulos etal, 2010; Bayindir etal, 2015; Ghandour etal, 2016; Babaei etal, 2017)."
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"Additionally, activation of PPARgamma has been shown to promote myeloid differentiation [XREF_BIBR] possibly limiting the accumulation of MDSC and evidence shows that PPARgamma agonists can alleviate macrophage suppression of cytotoxic T lymphocytes [XREF_BIBR], further suggesting that targeting PPARgamma may diminish tumor associated suppressive mechanisms."
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"13 In order to determine whether TZDs or obesity affect PPARgamma mediated prostatic differentiation in vivo, we fed male mice a Western diet or Rosiglitazone chow for 6 months and examined their prostates for changes in morphology (XREF_FIG) and PPARgamma regulated genes (XREF_TABLE)."
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"GCM-1 may be regulated by the transcription factor peroxisome proliferator activated receptor-gamma (PPAR-gamma); in mice, PPAR-gamma promotes labyrinthine trophoblast differentiation via Gcm-1, and, as we previously demonstrated, PPAR-gamma activation ameliorates disease features in rat model of preeclampsia."
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"PPARgamma activation has been shown to inhibit proliferation, promote differentiation and induce apoptosis in various malignant tissues; and its agonists have been used as therapeutic agents for psoriasis, a benign skin disease characterized by epidermal hyperplasia [XREF_BIBR, XREF_BIBR - XREF_BIBR]."
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"In other systems, it was shown that osteoclast specific PPARgamma knockout mice are characterized by increased bone mass due to impaired osteoclast differentiation [XREF_BIBR], suggesting antagonistic effects of PPARgamma and MEK1 on different bone cell types : with PPARgamma promoting osteoclast differentiation, and MEK1 inhibiting chondrocyte differentiation."
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"Except for its roles in lipogenesis, the activation of PPARgamma also promotes terminal differentiation, which is achieved through the induction of a variety of differentiation dependent genes that are crucial for fatty acid uptake and storage, such as FABP4, LPL and others [XREF_BIBR]."
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"FSB (1 mug/ml) showed similar effects, that is, it inhibited PPARgamma induced adipocyte differentiation (66.3 +/- 5.12% reduction in rosiglitazone induced adipogenesis; 53.3 +/- 2.53% reduction in pioglitazone induced adipogenesis) (XREF_FIG) and target gene expressions (XREF_FIG)."
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"In monocytes, PPARgamma stimulates osteoclast differentiation through peroxisome proliferator activated receptor gamma, coactivator 1, beta (PGC-1beta)-dependent mechanism and activation of the c-Fos transcription factor, while, in MSCs, PPARgamma increases support for osteoclastogenesis by stimulating RANKL production [XREF_BIBR, XREF_BIBR]."
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"Adipocyte differentiation is driven by the expression and activation of three transcription factor families : the differentially expressed CAAT and enhancer binding proteins (C/EBPs) alpha, beta, and delta; the helix-loop-helix adipocyte differentiation and determination factor-1; and peroxisome proliferator activated receptor gamma (PPARgamma), expressed as two isoforms, PPARgamma1 and the adipocyte specific PPARgamma2."
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"Although their functional roles in the PPARgamma transcriptional pathway are not well defined, we recently found that production of cyclic phosphatidic acid (cPA), a simple phospholipid, inhibits transcription of PPARgamma target genes that normally drive adipocytic differentiation, lipid accumulation in macrophages, and arterial wall remodeling [XREF_BIBR]."
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"Considering the fact that several BMPs, in coordination with other signaling molecules, have been shown to stimulate preadipocyte differentiation, we hypothesized that the PPARgamma agonist enhances osteoblastic differentiation of cultured human periosteum derived cells by activating BMP signaling XREF_BIBR, XREF_BIBR."
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"To reach PPARgamma induced maturity of the adipocyte differentiation there are known to be modulated by some stimulators including PGs, insulin like growth factor 1 (IGF-1), insulin, cAMP, triiodothyronine, macrophage colony stimulating factor, fatty acids, and glucocorticoids XREF_BIBR, XREF_BIBR, as well as inhibitors including glycoproteins, transforming growth factor-beta (TGF-beta), inflammatory cytokines and growth hormone 18."
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"In the present study, we utilized rosiglitazone, a potent peroxisome proliferator activated receptor gamma agonist, to induce adipogenic differentiation of OP9-DL1 cells, and detected the metabolomics alterations during adipogenic differentiation by using liquid chromatography-mass spectrometry."
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"On the one hand, Ppargamma favours the differentiation of mesenchymal stem cells into adipocytes rather than osteoblasts or chondrocytes XREF_BIBR; Ppargamma overexpression has been reported to promote adipogenic differentiation in growth plate chondrocytes XREF_BIBR, but it has no effect on fully differentiated osteoblasts or osteoclasts XREF_BIBR."
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"Here, we demonstrate that repeated administrations of PPAR-gamma agonists to OP cultures accelerate their differentiation to OLs, as indicated by increased numbers of O4- and O1 positive cells that show increased myelin basic protein expression, elaborated cholesterol-enrichedmembranes and have increased peroxisomes."
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"Previously, we demonstrated that PPAR-alpha ligands (clofibrate and ciprofibrate) and PPAR-gamma ligands (troglitazone and 15d-prostaglandin J2) inhibit growth and induce monocytic differentiation in HL-60 cells, and HNE, which alone induces granulocytic like differentiation of HL-60 cells, potentiates the monocytic differentiation induced by ciprofibrate, troglitazone, and 15d-prostaglandin J2."
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"Herein, we cultured primary thymic stromal cells (TSCs), used rosiglitazone, a potent peroxisome proliferator-activated receptor gamma (PPARgamma) agonist, to induce adipogenic differentiation, and investigated the differentially expressed genes during adipogenic differentiation by using RNA-sequencing analysis."
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"Another PPARgamma agonist, ciglitazone, has been shown to increase regulatory T (Treg) cell differentiation from naive T cells XREF_BIBR, while pioglitazone has been demonstrated to ameliorate EAE severity through selective inhibition of Th17 differentiation XREF_BIBR and inhibit human alloresponses in a humanized model of graft arteriosclerosis XREF_BIBR."
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"PPARgamma, the master regulator of adipogenesis, cooperates with C/EBPalpha to initiate adipogenic differentiation, is required in human preadipocyte differentiation [XREF_BIBR, XREF_BIBR], and can increase glycerol-3-phosphate dehydrogenase (GPDH) activity in sheep preadipocytes [XREF_BIBR], an enzyme involved in lipid biosynthesis."
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"Accumulating evidence indicates that PPARgamma promotes cell differentiation following activation by its ligand [XREF_BIBR - XREF_BIBR] and since telomerase is not active in differentiated cells [XREF_BIBR, XREF_BIBR], we wondered if the inhibition of telomerase by troglitazone is the result of cell differentiation."
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"Based on the finding that PPARgamma is expressed in growth plate chondrocytes [XREF_BIBR], as well as the evidence that PPARgamma is able to compete with the thyroid hormone receptor (TR) for binding to retinoic acid receptor X to inhibit growth plate cell hypertrophy [XREF_BIBR], the purpose of this study was to investigate whether PPARgamma and its ligands are able to promote adipogenic differentiation and suppress chondrogenic differentiation in growth plate chondrocytes."
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"C/EBPbeta cooperates with the positive regulatory domain containing 16 (PRDM16) to induce brown fat determination and differentiation, which subsequently leads to activation of thermogenic genes such as adrenergic receptor beta3 (Adrb3), peroxisome proliferator activated receptor gamma coactivator 1alpha (Pgc1a), and mitochondrial uncoupling protein 1 (Ucp1) [XREF_BIBR, XREF_BIBR]."
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"Moreover, we revealed that exon 3 skipping, which causes no frame shift but loss of a domain essential for nuclear translocation, was affected by pioglitazone, a highly selective activator of the peroxisome proliferator activated receptor gamma (PPARgamma) which contributes to cell differentiation and tumorigenesis besides its metabolic actions."
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"For example, activation of the nuclear receptor peroxisome proliferator activated receptor gamma (PPAR-gamma) by its synthetic ligand rosiglitazone, a widely used anti-diabetes drug in the thiazolidinedione (TZD) class, can promote adipocyte differentiation but inhibit osteoblast differentiation, which contributes to its bone loss side effect together with its ability to enhance osteoclastogenesis and bone resorption (XREF_FIG)."
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"In contrast, ONO-4819 reduced the mRNA expression of peroxisome proliferator activated receptor gamma (PPARgamma) and inhibited adipocyte differentiation of C3H10T1/2 cells, which findings are consistent with the observation that the age dependent increase in adipocyte number in the bone marrow was significantly suppressed in the ONO-4819-treated animals."
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"In another leukemic cell line, U937 cells, PPARgamma ligands inhibited proliferation but did not induce differentiation (except the higher doses of 15d-PG J2 which induced a poor monocytic differentiation) [XREF_BIBR] indicating that the differentiation induction by PPAR ligands is cell-type specific."
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"Therefore, it should not be surprising that in line with the previous work, nebulized PGZ stimulated alveolar maturation and protection against hyperoxia induced neonatal lung injury, since lipofibroblast differentiation is driven by PPARgamma, and since lipofibroblasts are known to be cytoprotective against oxidant injury, and produce specific growth and differentiation and homeostasis."
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"PPARgamma stimulates trophoblast differentiation to activate downstream target genes [XREF_BIBR, XREF_BIBR], and this regulation process is mainly mediated through chorion specific transcription factor-1 (GCM-1) and the increased expression of chorionic gonadotropin beta-subunit (hCGbeta)."
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"After stem cell commitment toward white adipocyte lineage, the expression and activation of PPARgamma is both sufficient and crucial to initiate the adipogenic differentiation program and maintain adipocyte phenotype, integrity, and function, based on a large set of different genetic mouse models."
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"PPARgamma signaling in cancer has been shown to upregulate differentiation markers, CDK inhibitors (p21 and p27), and apoptosis markers while PPARgamma has been shown to inhibit inflammatory markers (COX-2, cytokines, and inducible nitric oxide synthase), PI3K and Akt activity, and angiogenesis [XREF_BIBR]."
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"Finally, PPARg activation directly promotes oligodendroglial differentiation, enhances oligodendroglial survival, promotes myelin gene expression XREF_BIBR - XREF_BIBR, suppresses the inflammatory responses and reactive oxygen and nitrogen species and increases cellular anti-oxidants 34 in oligodendrocytes."
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"The thiazolidinedione (TZD) or glitazone class of peroxisome proliferator-activated-gamma (PPAR-gamma) ligands not only induce adipocyte differentiation and increase insulin sensitivity, but also exert growth inhibitory effects on several carcinoma cell lines in vitro as well as in vivo."
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"Moreover, several studies have revealed a differential DNA methylation pattern in IPF lung and control samples XREF_BIBR, XREF_BIBR, XREF_BIBR, describing a hypermethylation of specific genes, such as CD90 XREF_BIBR, XREF_BIBR and PPAR-gamma XREF_BIBR, XREF_BIBR, XREF_BIBR (whose silencing is DNMTs- and HDACs dependent 37), which contributes to myofibroblast differentiation."
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"Together with adipogenic cocktail, activation of PPARgamma via exogenous ligands such as rosiglitazone or TBT strongly promotes adipocyte differentiation and maintenance, together with the expression of genes involved in lipid droplet formation, glucose uptake, fatty acid synthesis, and adipokine secretion XREF_BIBR, XREF_BIBR."
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"It has been proposed that the insulin sensitizing activity of PPARgamma activation may be mediated via a range of pathways, including the following : enhanced adipocyte differentiation; altered expression of key intermediates such as GLUT4, IRS1, IRS2, PI3K P85, and PTEN; reduced production of inflammatory cytokines; altered GLUT4 recycling; reduced oxidative stress; increased mitochondrial biogenesis; and inhibition of mitochondrial respiration."
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"Researchers has found that after being activated by ligand, PPARgamma can induce tumor cell differentiation, repress their proliferation, promote their apoptosis, and concomitantly reduce neoplastic angiogenesis, which eventually halts the tumor growth, proliferation, infiltration, and metastasis [XREF_BIBR, XREF_BIBR]."
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"In conclusion, although further study will be needed to clarify the mechanisms of PPAR regulated osteogenesis, our results suggest that PPARgamma agonist stimulates osteoblastic differentiation of cultured human periosteal derived cells and PPARalpha and PPARgamma antagonists inhibit osteoblastic differentiation in these cells."
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"Consistent with the presence of lipid droplets, aP2 and PPARgamma, transcriptional factors which are required for adipogenesis, were up-regulated significantly after 3days in differentiation medium, demonstrating that the hffECM promotes differentiation of hESC under defined conditions."
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"The resulting fusion protein is believed to play a critical role in tumorigenesis, blocking the PPARgamma pathway which promotes adipocytic differentiation or maturation, offering insight into the primitive pre-adipocytic histological appearance of this tumor [XREF_BIBR, XREF_BIBR]."
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"In addition to its classical role as cell cycle promoter, cyclin D1 has been reported to be involved in cancer drug resistance by being suppressed by a miRNA (let-7b), to be essential for migration in macrophages [XREF_BIBR, XREF_BIBR] and might be indirectly involved in monocytic differentiation via inhibition of PPAR-gamma function [XREF_BIBR], as the PPAR-gamma and retinoid X receptor and alpha heterodimer in myelomonocytic cell lines is known to induce monocytic differentiation [XREF_BIBR]."
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"Detailed inspection of PPAR-alpha and PPAR-gamma crystal structures and molecular simulation supported the differentiation of most important descriptors in the separate PLS models, e.g. the higher impact of lipophilicity and bulk descriptors in PPAR-alpha and PPAR-gamma activity respectively, as well as the effect of specific structural descriptors."
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"In vitro studies show that activation of PPAR-gamma signaling by pioglitazone or other TZDs could promote differentiation of pluripotent mesenchymal stem cells into adipocytes at the expense of osteoblasts and suppress osteoblast differentiation and OC expression in osteoblastic cell lines [XREF_BIBR, XREF_BIBR]."
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"In cultured murine and human cells, PPARgamma agonists and overexpression of PPARgamma2 induce the differentiation of bone marrow stromal cells into the adipocyte lineage and negatively regulate osteoblast differentiation by repressing the osteoblast specific transcription factor Runx2 [XREF_BIBR - XREF_BIBR]."
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"PPARgamma mediated differentiation of normal human urothelial (NHU) cells in vitro requires coinhibition of epidermal growth factor receptor (EGFR) signalling and is characterised by de novo expression of late and terminal differentiation associated genes, including uroplakins (UPK), over a 6-day period."
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"In addition, TZD demonstrated potent inhibitory effects on the growth of PC cells via the PPARgamma dependent induction of ductal differentiation [XREF_BIBR], and the use of insulin glargine was not associated with an increased risk of all cancers or site specific cancers in Scotland over a 4-year time period [XREF_BIBR]."
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"Adipogenesis is regulated by the sequential activation of a series of transcription factors : the C/EBP proteins of type beta and delta trigger the process while PPARgamma and C/EBPalpha induce the differentiation from pre-adipocyte to adipocyte, followed by adipo specific gene expression."
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"We conclude that a PPARG-driven rapid differentiation switch is exclusively triggered in G1 to commit preadipocytes to differentiate and that the same differentiation switch simultaneously triggers permanent cell cycle exit with PPARG first inducing and then maintaining p21 expression."
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"Recent reports suggest that stimulation of PPARalpha, but not PPARbeta or PPARgamma, enhances cardiac progenitor differentiation through the involvement of NADPH oxidase activity XREF_BIBR, XREF_BIBR and that activation of PPARalpha induces neovascularization through a VEGF dependent mechanism XREF_BIBR, XREF_BIBR."
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"This work has demonstrated that (i) the activating C/EBPs and PPAR-gamma signaling pathways were sufficient to induce adipogenic differentiation from hMSC, (ii) D&R producing functional adipocytes from hMSC, (iii) D&R induce adipogenic differentiation from mammalian MSC (including those which are refractory to classical adipogenic differentiation stimuli)."
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"In addition, the fact that PPARgamma activation induces the differentiation of mesenchymal stem cells into adipocytes over osteoblasts suggests that PPARalpha could block PPARgamma signaling and therefore restore the differentiation into osteoblasts, which may benefit the treatment of diabetic osteoporosis with inhibition of PGC-1alpha and gluconeogenesis."
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"However, a number of fatty acid metabolism (Acsf2, Adipor1, Cd36, Lpl) and differentiation (AR, probasin) genes were equally high in prostate, including the glucose oxidation inhibitor, Pdk4, which suggests that the differentiation induced by PPARgamma expression shown here may represent a metabolically regulated program of prostatic differentiation in vivo."
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"Indeed, the majority of studies to date show that PPARgamma agonists can promote terminal differentiation, inhibit cell growth and increase apoptosis of human cancer cell lines; inhibit tumorigenesis in animal models of cancer; and in some cases PPARgamma agonists have shown modest efficacy for chemoprevention in clinical trials."
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"Although PPARgamma activation increases adipocyte differentiation that has a beneficial effect on increasing systemic insulin sensitivity and reducing hyperglycemia, its induction in the liver promotes hepatic steatosis, while deletion protects against HF-diet-induced hepatic steatosis."
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"In this study, we for the first time report that PPAR-γ interacts with Foxp3 to promote the differentiation of CD4 T cells into Treg cells and subsequently attenuating immunopathology during schistosome infection.The main pathology in schistosomiasis results from eggs deposited in the liver, which impacts on the hosts' living quality, health status, or even mortality [5]."
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"We used rosiglitazone, a potent peroxisome proliferator activated receptor gamma (PPARgamma) agonist, to induce adipogenic differentiation of OP9-DL1 cells, and investigated the differentially expressed proteins during adipogenic differentiation by using label-free quantitative proteomics."
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"Increased expression of the transcription factors PPARgamma and C/EBPalpha induces adipocyte differentiation by activating the expression of adipocyte specific proteins such as adiponectin, resistin, and apolipoprotein E, indicating that these transcription factors are important regulators of adipocyte differentiation [XREF_BIBR]."
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"In addition to the role of PPARgamma in glucose and lipid metabolism, PPARgamma stimulated adipocyte differentiation, and inhibition of PPARgamma attenuated adipocyte differentiation induced by breast cancer epithelial cells Furthermore, PPARgamma ligand therapy was tested in many preclinical studies of solid tumors, including breast cancer, showing a beneficial effect."
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"Recent studies demonstrated that in macrophages PPARgamma and STAT6 act in a cooperative fashion to induce the " alternative " pathway of activation and differentiation into M2-type activated cells, while another transcription factor HIF-1alpha mediates the " classical " activation pathway giving rise to M1-type cells."
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"PPARgamma ligands also promote terminal differentiation of malignant breast epithelial cells in vitro, induce apoptosis and fibrosis of injected breast tumor cells (MCF-7) in mice, and reduce tumor incidence in rats treated with nitrosomethylurea and in mice injected with prostate tumor cells (PC-3) [XREF_BIBR]."
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"Due to the modulatory role of PPARgamma in the differentiation of monocytes and monocyte derived macrophages, both natural and synthetic agents targeted PPARgamma could promote the differentiation of monocytes towards a M2 phenotype and improve the outcome of SLE, which may be an adjuvant to the treatment of this complicated autoimmune disease [XREF_BIBR, XREF_BIBR]."
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"Our results demonstrate that KMP fortifies TAZ activity, which enhances RUNX2 mediated osteoblast differentiation and suppresses PPARgamma stimulated adipocyte differentiation, indicating the potential of KMP as an effective therapeutic reagent for controlling bone loss and adiposity through TAZ activation."
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"XREF_BIBR, XREF_BIBR PPARgamma activation upon ligand binding is critical for the expression of genes such as adiponectin and fatty acid binding protein (FABP) (also referred as aP2) involved in adipocyte differentiation and lipid metabolism XREF_BIBR, XREF_BIBR While enforced PPARgamma expression induces adipocyte differentiation from fibroblasts, PPARgamma-deficiency attenuates white adipose tissue development."
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"We have previously shown that natural (15-deoxy-Delta-prostaglandin J2) and synthetic (pioglitazone) agonists of peroxisome proliferator activated receptor gamma (PPAR-gamma) strengthen the intrinsic cellular mechanisms protecting oligodendrocyte (OL) progenitors (OPs) from oxidative insults and promote their differentiation."
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"The concept that cyclin D1 regulates PPARgamma function has additional implications for breast cancer, wherein PPARgamma is known to promote breast epithelial cell differentiation, and histological analyses of breast cancer specimens revealed that PPARgamma is reduced in tumors with a high cyclin D1 index [XREF_BIBR, XREF_BIBR]."
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"In the already mentioned work by Han et al., in which the presence of PPARgamma in NB cells was described for the first time, the authors also demonstrated that the synthetic PPARgamma agonist GW1929 induced the differentiation of LA-N-5 cells and inhibited cell proliferation [XREF_BIBR]."
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"XREF_BIBR, XREF_BIBR In a recent report, high-fat diet induced accumulation of large adipocytes promoted peroxisome proliferator activated receptor gamma activated differentiation factors, which resulted in elevated G-protein-coupled receptor 43 expression in subcutaneous adipose tissue."
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"This view is consistent with an earlier report in which the PPARgamma selective ligand was unable to increase PPARgamma expression and cause adipocyte differentiation in human adult trabecular derived bone cells, although these cells were able to undergo adipogenesis in the presence of isobutylmethylxanthine (IBMX) plus dexamethasone with concomitant increase in expression of PPARgamma [XREF_BIBR]."
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"The pharmacological activation of PPARgamma using specific ligands increases the proliferation and differentiation of neural stem cells in specific brain regions, including the hippocampus, and prevents neurodegeneration and improves cognition and anxiety and depression like behaviors in animal models."
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"It is worth noting that PPARgamma and PPARbeta and delta cooperatively function to induce differentiation of adipocytes in vitro, facilitated by PPARgamma [XREF_BIBR], but this new study [XREF_BIBR] shows that in differentiated adipocytes, activating PPARbeta and delta causes distinctly different effects from those resulting from activating PPARgamma."
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"In order to identify key regulators in thymic adipogenesis, the present study used rosiglitazone, a potent peroxisome proliferator activated receptor gamma (PPARgamma) agonist, to induce adipogenic differentiation of OP9-DL1 cells, and investigated the differentially expressed proteins during adipogenic differentiation by using label-free quantitative proteomics."
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"For example, peroxisome proliferator activated receptor gamma (PPARgamma) drives the differentiation of mesenchymal stem cells into adipocytes, while Runt related transcription factor 2 (Runx2) and sex determining region Y (SRY)-box transcription factor 9 (SOX9) drive differentiation into osteochondroprogenitor cells (XREF_FIG) [XREF_BIBR]."
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"These results indicated that the activation of PPAR-γ by an agonist could directly promote differentiation of CD4 T cells into Treg cells.To determine whether PPAR-γ promoted CD4 T cell differentiation through interaction with Foxp3, CD4 T cells were prepared and stimulated with pioglitazone in vitro."
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"Moreover, VGVAPG peptide decreased lipid accumulation measured by ORO assay and increased the expression of Pref-1, serpin E1 and adiponectin as compared to that in rosiglitazone (PPARgamma agonist used to trigger differentiation of 3T3-L1 cells)-treated group, while simultaneously decreasing the expression of VEGF and resistin."
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"Alternatively, terminal differentiation may be induced pharmacologically by activation of PPARgamma with concurrent inhibition of EGFR; this initiates a programme of transcriptional changes that results in expression of a late and terminal differentiated urothelial cell phenotype XREF_BIBR, XREF_BIBR, XREF_BIBR."
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"For example, we identified changes in the MSC expression of the nuclear receptor PPARgamma that were consistent with earlier reports that indicated PPARgamma is both requisite and sufficient to induce terminal adipocyte differentiation 25 and that oxidants amplify PPARgamma expression."
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"By leveraging primary oligodendrocyte progenitor cells (OPCs), microglia depleted mice, and conditional OPC specific peroxisome proliferator activated receptor gamma (PPARgamma) knockout mice, we discovered a direct salutary effect of IL-4 on oligodendrocyte differentiation that was mediated by the PPARgamma axis."
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"Activation of the nuclear hormone receptor peroxisome proliferator activated receptor gamma (PPARgamma) inhibits cell growth and induces differentiation in both adipocyte and epithelial cell lineages, although it is unclear whether this occurs through common or cell-type specific mechanisms."
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"Moreover, a relevant PPAR-gamma effect on bone differentiation and metabolism, based on the ability to trigger and switch differentiation of progenitor cells towards adipogenesis at the expense of osteogenesis, and possibly on mechanisms involving osteoclast mediated bone resorbtion, is also taking place."
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"In addition, glucocorticoids increase production of peroxisome proliferator activated receptor gamma, a transcription factor that induces terminal adipocyte differentiation while suppressing osteoblast differentiation, potentially contributing to increased marrow fat and reduced osteoblasts."
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"Steroids can also stimulate the expression of PPARgamma mRNA both in vivo and in vitro, and increased PPARgamma expression can reduce osteogenic differentiation, induce adipogenic differentiation, promote bone marrow adiposity, rise intraosseous pressure, block local blood perfusion, and finally lead to osteonecrosis."
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"It seems highly possible, since several in vitro studies have revealed that pioglitazone, a PPAR-gamma agonist, induces cell differentiation [XREF_BIBR] and several clinical studies have demonstrated that the activation PPAR-gamma increases the degree of histopathological differentiation of liposarcoma [XREF_BIBR, XREF_BIBR]."
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"Our finding that pioglitazone favorably affects the dyslipidemic effect of CSA is consistent with reports that activation of PPARgamma induces monocyte and macrophages differentiation and uptake of ox-LDL [XREF_BIBR] and inhibits the production of inflammatory enzymes such as iNOS and matrix metalloproteinase-9 [XREF_BIBR], and pro inflammatory cytokines such as TNF-alpha, IL-1beta, IL-6 [XREF_BIBR]."
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"Adipogenesis is orchestrated by transcriptional program where the master regulator is Ppargamma that works in concert with other transcriptional regulators, most notably the CAAT enhancer binding proteins transcription factor family to promote adipocyte differentiation (XREF_FIG A) XREF_BIBR."
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"The nuclear receptor peroxisome proliferator activated receptor gamma (PPARgamma) promotes adipocyte differentiation, exerts atherogenic and anti-inflammatory effects in monocyte and macrophages, and is believed to mediate the insulin sensitizing action of antidiabetic thiazolidinedione ligands."
reach
"TBT activates both PPARgamma and RXR inducing differentiation of adipocytes [XREF_BIBR, XREF_BIBR, XREF_BIBR] but not all the health promoting activities induced by PPARgamma and in particular not the pathways linked to mitochondrial biogenesis or those involved in beiging [XREF_BIBR]."