IndraLab
Statements
Lipopolysaccharide activates JNK. 655 / 677
|
9
1
644
1
reach
"Finally, further study is warranted to define the relationship of PI3K and Syk to the Tec kinases in the pathway leading to LPS induced JNK activation in neutrophils, since PI3K and Syk reside upstream of JNK in this pathway [XREF_BIBR] and are upstream of the Tec kinases in other cell systems [XREF_BIBR, XREF_BIBR]."
reach
"Xanthoangelol is a phytochemical that attenuates LPS induced c-Jun N-terminal kinase (JNK) phosphorlyation in macrophages, lowers macrophage infiltration into subcutaneous white adipose tissue, improves glucose tolerance, and increases UCP-1 expression in diet induced obesity (DIO) mice 55 but has not advanced to clinical trials in humans to date."
reach
"Importantly, we observed that the direct induction of cell death and activation of JNK signaling by LPS on hepatocytes were rather minor, raising the possibility that the severe in vivo liver cell death caused by LPS was triggered by additional factors such as TNF-alpha that is known to be produced mainly by macrophages which was much enriched in the livers in sepsis (XREF_FIG)."
reach
"Furthermore, expression of a catalytically inactive form of MKP-M in a mouse macrophage cell line increased the intensity and duration of JNK activation and TNF-alpha secretion after LPS stimulation, suggesting that MKP-M is at least partially responsible for the desensitization of LPS mediated JNK activation and cytokine secretion in macrophages."
reach
"Interestingly, a JNK inhibitor (SP600125) and another tyrosine kinase inhibitor (genistein) significantly inhibited STAT-1 phosphorylation, suggesting that the LPS activated JNK pathway and a tyrosine kinase pathway (especially Tyk2) may link to the STAT-1 pathway, which is involved in iNOS induction."
reach
"The JNK kinase activity in response to adherent (P + Opa -) or invasive (P - Opa +) Ngo strains, which induce a variety of proinflammatory cytokines, was observed rapidly within 15 min after infection at a MOI of 50 and further increased within 90 min, whereas the nonpathogenic strain (P - Opa -) or LPS induced weak and no JNK activity, respectively."
reach
"Meanwhile, LIPUS treatment effectively suppressed the LPS induced production of tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, inducible nitric oxide synthase, and cyclooxygenase-2 in the microglial cells, in addition to inhibiting the LPS induced expressions of toll like receptor 4 and myeloid differentiation factor 88, as well as the LPS induced activation of c-Jun N-terminal kinase and nuclear factor kappa B. Furthermore, LIPUS significantly decreased the Bax and Bcl -2 ratio in the microglia following LPS treatment."
reach
"We found that selonsertib pretreatment effectively prevented LPS induced activation of JNK and DRP1 and mitochondrial dysfunction in primary hepatic macrophages and macrophagic cell line and also suppressed the release of the proinflammatory cytokines TNF-alpha and IL-1alpha, which are known as major cytokines causing liver injury and inflammation [XREF_BIBR, XREF_BIBR]."
reach
"Although MAPKs can transmit environmental stimuli into the nucleus to regulate the activity of cytokines or other inflammatory mediators such as TNF-alpha, IL-6 and NO, in this study, DMY treatment did not have a discernable effect on LPS induced activation of JNK and ERK proteins, as revealed by no changes in levels of phospho-JNK and phospho-ERK protein in macrophages."
reach
"These findings indicated that MSCs can support T-cell functions by regulating MAPK-ERK/JNK signaling.The lipopolysaccharide (LPS)-induced acute lung injury model demonstrates a severe immune response characterized by diffuse interstitial and alveolar edema, inflammatory cell infiltration, and the release of proinflammatory factors, which are similar to the symptoms of COVID-19 caused by the rapid replication of SARS-CoV-2 in the lungs.30,31 We next investigated the effect of MSCs on lung injury repair."
reach
"In contrast, however, macrophages isolated from either XLA patients [XREF_BIBR] or Btk deficient mice [XREF_BIBR] show normal levels of JNK phosphorylation after LPS stimulation, suggesting that either other, non Btk, Tec kinases regulate LPS induced JNK activation in macrophages or that LPS induced JNK activation in macrophages is independent of the Tec kinases."
reach
"We show here that both Tec and Btk are activated in human neutrophils stimulated with LPS, that Tec kinases are upstream in the LPS induced pathway regulating JNK, but not p38, activity, and that actin assembly and cytokine production in LPS stimulated human neutrophils is dependent on activation of the Tec kinases."
reach
"These findings indicated that MSCs can support T-cell functions by regulating MAPK-ERK/ JNK signaling.The lipopolysaccharide (LPS)-induced acute lung injury model demonstrates a severe immune response characterized by diffuse interstitial and alveolar edema, inflammatory cell infiltration, and the release of proinflammatory factors, which are similar to the symptoms of COVID-19 caused by the rapid replication of SARS-CoV-2 in the lungs."
reach
"However, that the action of the antiviral factors in supernatants of LPS activated cells is independent of both p38 MAPK and JNK, since MDM treated with LPS supernatants were resistant to ADA infection, despite being infected and cultured in the presence of the kinase inhibitors (XREF_FIG)."
reach
"ERK, JNK, and p38 MAP kinases are activated by LPS in microglia and inhibition of a respective kinase with pharmacological inhibitors : CEP11004 or CEP-1347 reduced cytokine production in LPS stimulated human and murine microglia cultures [XREF_BIBR, XREF_BIBR] or exposed to neurotoxic peptide Abeta1-40 [XREF_BIBR]."
reach
"The amplified inflammatory cytokines were reduced in the presence of P38 inhibitor or JNK inhibitor (Supplementary Fig. 1b,c), indicating that P38 and JNK might also be essential for RIPK1- and RIPK3-mediated inflammatory signaling pathway.To further confirm the roles of P38 and JNK in RIPK1- and RIPK3-induced inflammatory signaling pathway, we analyzed the activation of P38 and JNK and found that LPS plus zVAD induced more P38 and JNK activation compared with those induced by LPS alone (Fig. 1a)."
reach
"Whereas JNK is activated by LPS [XREF_BIBR] and TNF-alpha [XREF_BIBR] only in non suspended adherent cells, likely due to the requirement for beta 2 integrin ligation [XREF_BIBR], LPS- [XREF_BIBR] and TNF-alpha-induced [XREF_BIBR] p38 activation is present in suspended neutrophils."
reach
"Furthermore, the water extract, but not the ethanol extract, of ES dose-dependently inhibited LPS-induced JNK, p38 mitogen-activated protein kinases (MAPK), and slightly inhibited cyclooxygenase (COX-2) in BV-2 cells but decreased p38 MAPK and COX-2 expressions in the liver of LPS-treated rats."
reach
"d-GalN/LPS treatment resulted in a marked inflammatory cytokine release and stimulated the activation of signal transducer and activator of transcription (STAT) 3, c-Jun N-terminal kinases (JNK) and extracellular signal-regulated kinase (ERK) signaling comparably in the hepatic compartment of Bcl-3 Hep and WT mice."
reach
"In the present study, we further found that melittin and bee venom significantly reduced inflammatory stimuli (LPS and SNP)-induced activation of JNK signal, and the JNK signal specific inhibitor SP600215 suppressed the inhibitory effect of melittin and bee venom on the NF-kappaB activation, and inflammatory reaction in Raw 264.7 macrophages and synoviocytes obtained from rheumatoid arthritis patients."
reach
"LPS induced cleavage (activation) of caspase-3, an indicator of apoptotic change, and increased protein expression of proapoptotic molecules, Bax and Bim, and activation of c-Jun NH 2 -terminal kinase (JNK and SAPK) in the liver and spleen were attenuated by both simvastatin and FTI-277."
eidos
"LPS activates ERK1 / 2 , JNK , and p38 MAPK , which ultimately control the activity of transcription factors regulating the expression of inflammation modulators , such as induced NO synthase ( iNOS ) , cyclooxygenase-2 ( COX-2 ) , TNF-alpha , IL-1alpha , IL-1beta , and IL-6 [ 44 ] ."
| PMC
reach
"Similar results are described by Kim et al. [122] for 6,6bieckol, which can reduce, depending on the dose, the expression of iNOS, COX-2, and pro-inflammatory cytokines in LPS-stimulated RAW 264.7 cells and BV2 microglial culture cells through the inhibition of the IκB-α/NF-kB and JNK pathways/ p38 MAPK/Akt, in connection with which this PTs can become the basis of a therapeutic agent for the treatment of neuroinflammatory diseases in the future [122] ."
reach
"In cultured podocytes, AdipoRon attenuated the LPS induced activation of the central inflammatory signalling pathways NF-kappaB-p65, c-Jun N-terminal kinase (JNK) and p38 mitogen activated protein kinase (p38-MAPK) (30%, 36% and 22%, respectively, p < 0.001), reduced the secretion of TNFalpha (32%, p < 0.01), and protected against podocyte apoptosis and migration."
reach
"In addition, using Dox induced Tet-On H9c2 myocardial cells and ERalpha transfected cardiomyocytes to overexpress ERalpha, we observed that activation of the PI3K-Akt signalling pathway is required for E 2, BSA-E 2 and/or ERalpha to significantly abolish the LPS induced JNK1/2 activation, IkappaB degradation, NFkappaB activation and subsequent increases in pro apoptotic proteins and apoptosis in myocardial cells."
reach
"The current study was designed to test the hypothesis that TIPE2 attenuates LPS-induced ALI through the inhibition of lung inflammation and apoptosis, which may be associated with suppressing NF-κB and JNK activation.Reagents LPS (E. coli 0111:B4) was obtained from Sigma-Aldrich (St. Louis, MO)."
reach
"In this model, LPS stimulates alveolar macrophages via the TLR4/CD14/MD2 complex and the MyD88-dependent response, and activates nuclear factor kappa B (NF-κB) and c-Jun N-terminal kinase (JNK) that regulate the secretion of inflammatory mediators such as cytokines (e.g., IL-8, TNF-α, IL-1β, and IL-6) (3)."
reach
"Ajizian et al. (1999) suggested that activation of ERK is thought to be involved in LPS induced macrophage responses XREF_BIBR; in addition, JNK and p38 are activated by LPS stimulation and they have been postulated to play important roles in controlling iNOS gene expression XREF_BIBR."
reach
"We found that LPS induced IL-12 p40 protein and mRNA in a time- and concentration dependent manner in PMA treated THP-1 macrophages, and that LPS activated JNK and p38 mitogen activated protein (MAP) kinase, but not extracellular signal regulated kinase, in PMA treated THP-1 cells."
reach
"LPS can interact with TLR2, a major member of the TLR family, to activate the downstream protein nuclear factor-κB (NF-κB), P38 mitogen-activated protein kinase (MAPK) and C-Jun N-terminal kinase (JNK) of TLR2 and regulate the production of LPS-induced pro-inflammatory cytokines such as IL656."
reach
"LPS stimulation of human monocytes activates several intracellular signaling pathways that include the IkappaB kinase (IKK) and nuclear factor-kappaB (NF-kappaB) pathway and three mitogen activated protein kinase (MAPK) pathways : extracellular signal regulated kinases 1 and 2 (ERK1/2), c-Jun N-terminal kinase (JNK) and p38 [XREF_BIBR]."
reach
"Pretreating murine macrophages (RAW 264.7) with luteolin inhibited LPS stimulated TNFalpha and IL-6 release, which was associated with blockage of LPS induced activation of nuclear factor kappa B (NF-kappaB) and mitogen activated protein kinase (MAPK) family members ERK, p38, and JNK [XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR]."
reach
"Because ligation of TLR4 triggers the activation of MAP kinase and NF-kappaB, leading to production of proinflammatory cytokines through the MyD88 dependent pathway, we investigated the activation of MAP kinase such as JNK, p38, and ERK1/2 in macrophages treated with LPS or 2,000 kDa gamma-PGA."
reach
"Such antioxidant activities can contribute to immunoregulatory and anti-inflammatory abilities.Furthermore, the results indicated that both hyalomin-A1 and B1 significantly suppressed the LPS-induced activation of the JNK subgroup of the MAPK signaling pathway by blocking JNK phosphorylation and, consequently, led to a reduction in MCP-1, IFN-γ, and tumor necrosis factor-α genes."
reach
"These results suggested that CuEO exerted anti-inflammatory effects in LPS stimulated RAW 264.7 cells via inhibition of NF-kappaB and mitogen activated protein kinases ERK and JNK signaling; the chemical could be used as a source of anti-inflammatory agents as well as dietary complement for health promotion."
reach
"We show that treatment of differentiated THP-1 cells with purified Stx1 resulted in prolonged activation of c-Jun N-terminal kinase (JNK) and p38 mitogen activated protein kinase (MAPK) cascades, and lipopolysaccharides (LPS) rapidly triggered transient activation of JNK and p38 and prolonged activation of extracellular signal regulated kinase cascades."
reach
"These derivatives of G-Rh2 reduce LPS induced production of TNF-alpha, IL-6, and IL-1beta as well as the activities of p38 MAPK, JNK, and NF-kappaB, showing greater anti-inflammatory effects than that of G-Rh2 XREF_BIBR, XREF_BIBR, in turn suggesting that improving bioavailability and water solubility of ginsenosides could also improve their anti-inflammatory effects."
reach
"To confirm the nuclear translocation results, phosphorylation level of JNK, p38 and NF-kappaB p65 were detected by Western blotting, which showed that JNK and c-Jun, p38, and NF-kappaB signalings were remarkably activated by 10mug/mL LPS and 100mug/mL ox-LDL, but not by 100mug/mL CHC except a slight up-regulation of p-JNK."
reach
"For example, berberine suppressed the activation/phosphorylation of p38, JNK, and ERK and suppressed the expression of IL‑1β, IL‐6 in LPS‐stimulated macrophages.29, 30 Hesperidin inhibited LPS‑induced activation of JNK and p38 MAPK pathways and prevented LPS‐induced endotoxicity in rats."
reach
"We have previously shown that inducible inflammatory mediator production is inhibited by a post-transcriptional mechanism, since mycolactone does not modulate the LPS dependent activation of ERK, JNK, p38 MAPK or NFkappaB and induced levels of mRNA are maintained or even enhanced XREF_BIBR."
reach
"At concentrations of 0.5, 0.75, and 1mg/mL, treatment with BPTS inhibited levels of expression of LPS induced NF-kappaB and MAPKs (ERK, JNK, and p38) as well as production of proinflammatory mediators, such as nitric oxide (NO), prostaglandin E 2 (PGE 2), tumor necrosis factor-alpha (TNF-alpha), and interleukin-6 (IL-6) by LPS."
reach
"In addition, Cortex Phellodendri inhibited inducible nitric oxide synthase (iNOS), activated nuclear factor-kappaB (NF-kappaB) by degradation and phosphorylation of IkappaBalpha, and attenuated phosphorylation of mitogen activated protein kinases such as ERK1/2, p38, and JNK in mice treated with lipopolysaccharide [XREF_BIBR]."
reach
"LPS induced cleavage (activation) of caspase-3, an indicator of apoptotic change, and increased protein expression of proapoptotic molecules, Bax and Bim, and activation of c-Jun NH 2 -terminal kinase (JNK and SAPK) in the liver and spleen were attenuated by both simvastatin and FTI-277."
reach
"CPT-2-Me-cAMP also prevented LPS induced activation of JNK and inhibition of AKT Taken together, these results suggest that LPS can induce hepatocyte apoptosis directly in vitro in a JNK dependent manner and activation of cAMP-GEF protects against the LPS induced apoptosis most likely by reversing the effect of LPS on JNK and AKT Introduction."
eidos
"In this model , LPS stimulates alveolar macrophages via the TLR4 / CD14 / MD2 complex and the MyD88-dependent response , and activates nuclear factor kappa B ( NF-kappaB ) and c-Jun N-terminal kinase ( JNK ) that regulate the secretion of inflammatory mediators such as cytokines ( e.g ., IL-8 , TNF-alpha , IL-1beta , and IL-6 ) ( 3 ) ."