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"In addition, in prostate cancer cells TGF-beta1 stimulates the expression and activity of uPA, PAI-1, and MMP-9, resulting in a net increment of pericellular plasminogen activation, increased activation of MMP-9, and finally increased tumour cell invasion and metastasis [XREF_BIBR, XREF_BIBR]."
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"Our current understanding of the pathways utilized by the TGF-beta1 to stimulate the PAI-1 transcription (summarized in XREF_FIG) indicate that this growth factor activates a kinase cascade, at least partially as a function of epidermal growth factor receptor mobilization (either through the release of the appropriate ligands or the direct receptor transactivation), involving MEK, ERK1/2, and perhaps p38 [XREF_BIBR - XREF_BIBR]."
"It seems that the tumor growth and invasion need both the profibrinolytic and procoagulant activities triggered simultaneously in different regions of the tumor or in different cells. PAI-1 expression in tumor cells is stimulated by TGF-beta which is itself activated by uPA-generated plasmin."
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"TAZ is required for maximal TGF-β1-mediated expression of the SMAD target gene encoding plasminogen activator inhibitor-1 (PAI-1), a potent profibrotic clade E member of the serine protease inhibitor family (SERPINE1) [ xref , xref , xref , xref ], and a similar involvement of YAP in TGF-β1-induced PAI-1 expression is evident in lung tumor cells [ xref ]."
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"atRA pretreatment effectively reduced fibronectin expression in glomerular mesangial cells stimulated with TGF-beta 1 or Ang II for 48 h. TGF-beta 1 stimulated PAI-1 expression reached a maximum at 5 h. atRA did n't affect the early (5 h) PAI-1 induction by TGF-beta 1, but markedly attenuated the sustained (48 h) PAI-1 induction."
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"Transforming growth factor-beta 1 (TGF-beta 1) rapidly increases the expression of junB transcription factor and plasminogen activator inhibitor-1 (PAI-1) and prevents the cell cycle dependent phosphorylation of the RB retinoblastoma susceptibility gene product during late G1 phase in Mv1Lu lung epithelial cells."
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"TAZ is required for maximal TGF-β1-mediated expression of the SMAD target gene encoding plasminogen activator inhibitor-1 (PAI-1), a potent profibrotic clade E member of the serine protease inhibitor family (SERPINE1) [27,28,29,30], and a similar involvement of YAP in TGF-β1-induced PAI-1 expression is evident in lung tumor cells [31]."
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"Consistent with these findings, p53 -/- fibroblasts are not inducible for increased PAI-1 expression in response to TGF-beta1 and pretreatment of Mv-1Lu mink lung cells (stably expressing a PAI-1 promoter-luciferase reporter construct) with the p53 inhibitor pifithrin-alpha effectively suppressed TGF-beta1-dependent PAI-1 transcription (XREF_FIG)."
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"Microphthalmia associated transcription factor (MITF), a member of the basic helix-loop-helix leucine zipper family of tissue specific transcription factors predominantly expressed in mast cells, melanocytes and osteoclasts, also stimulated PAI-1 gene transcription, and TGF-beta1 did not increase PAI-1 mRNA levels in mast cells from mi/mi mice expressing dominant negative MITF."
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"However, in primary cortical neurons, blocking of the serine protease HtrA1 (high temperature responsive antigen 1), which is known to regulate several pathologies, such as Alzheimer 's disease, macular degeneration, and osteoarthritis, led to overexpression of neuronal PAI-1 mediated by TGF-beta1 signaling and eventually to neuronal death."
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"A DN- pp60 c- src construct completely blocked TGF-beta1-initiated PAI-1 induction while TGF-beta1 failed to stimulate PAI-1 expression in SYF -/-/- fibroblasts; importantly, PAI-1 expression was restored in SYF -/-/- cells engineered to re-express a wild-type pp60 c-src construct."
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"In the present study, TGF-beta1 was shown to increase mRNA and protein levels of PAI-1 and decrease those of uPA, while APE significantly suppressed TGF-beta1-induced PAI-1 expression and increased uPA expression in the presence of TGF-beta1 in a dose dependent manner, therefore reversing the effects of TGF-beta1."
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"XREF_BIBR, XREF_BIBR, XREF_BIBR Overexpressed TGF-beta1 may increase the expression of PAI and TIMP-1, and simultaneously decrease the level of MMP-1 in the peritoneal mesothelial cell, which may result in decreased peritoneal fibrinolytic capacity and excessive deposition of ECM, and finally organizes to form dense adhesions."
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"Firstly, the PD model was established by TGF-beta1 stimulation in cultured HPMCs invitro, we found that TGF-beta1 significantly increased the EMT markers (alpha-SMA, vimentin, and fibronectin) and plasminogen activator inhibitor type 1 (PAI-1) expressions, but decreased epithelial marker (E-cadherin)."
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"TGF-beta1, by activating epidermal growth factor receptor (EGFR) signaling, stimulates the expression of the potent profibrotic matricellular plasminogen activator inhibitor-1 (PAI-1), which encodes the structural elements of ECM such as fibronectin and collagen 1 [XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR]."
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"The demonstration of a close correlation between the PAI-1 and TGF-beta 1 mRNA levels and the severity of lupus like glomerular lesions suggests that a pertubation of the glomerular PA/PAI balance, resulting from a marked TGF-beta 1 mediated induction of PAI-1 gene expression, plays an important role in the progression of lupus like glomerular lesions, leading to glomerulosclerosis."
"TGFbeta1 evoked gradual accumulation of PAI-1 protein in LX2 cells, with peak PAI-1 levels observed from 6?24h after stimulation (Fig 2A-B). Increases in PAI-1 protein content were preceded by increased expression of PAI-1 mRNA, and levels of PAI-1 mRNA remained about 3-fold increased for 24h (Fig 2C)."
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"In view of the similarities in the repertoire of participating signaling intermediates (e.g., EGFR, c-src, Rho and Rock, MEK/ERK1/2) between the microtubule- and TGF-beta1-initiated pathways of PAI-1 induction, and previous observations that TGF-beta1 expression is also regulated by cytoskeletal deformation [XREF_BIBR], it was important to determine if colchicine stimulated PAI-1 expression was mediated by an autocrine TGF-beta1 loop."