IndraLab
Statements
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"miR-130b was down-regulated, whereas TGF-betaR1, as well as the profibrotic genes collagen type IV alpha 1 (Col4a1), Col12a1, CTGF, and PAI-1 were up-regulated not only in mouse MC treated with TGF-beta1 but also in the glomeruli of streptozotocin injected diabetic mice, supporting in vivo relevance."
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"In contrast, TGFbeta1 upregulation of PAI-1 is not influenced by ED-A FN, indicating that the PAI-1 gene is regulated differently than alpha-SM actin and collagen type I. Interestingly, it has been shown that the increase of collagen type I and actin mRNA induced by TGFbeta1 is dependent on protein synthesis, whereas the induction of PAI-1 transcript is not."
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"Addition of authentic TGF-beta1 to parental cells greatly stimulated secretion of PAI-1 but not FN, whereas addition of TGF-beta antibody or lipofection with specific antisense TGF-beta1 oligonucleotides to EGR-1-regulated cells completely inhibits the secretion of PAI-1 but not FN."
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"It has been confirmed that TGF-beta1 induces PAI-1 synthesis, and a TGF-beta1 response element has been found in the promoter of the PAI-1 gene; in addition, multiple lines of evidence have determined that PAI-1 expression might be regulated in connection with several signaling pathways."
| PMC
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"We used esophageal biopsy specimens and plasma samples from control subjects and patients with EoE, primary human esophageal epithelial cells, and fibroblasts from patients with EoE in immunohistochemistry, quantitative PCR, and immunoassay experiments to understand the induction of PAI-1 by TGF-beta1, the relationship between PAI-1 and esophageal fibrosis, and the role of PAI-1 in fibrotic gene expression."
eidos
"Serpine1 expression is promoted by TGFbeta1 ( Honda et al ., 2017 ; Samarakoon & Higgins , 2008 ) and it is the major physiological regulator of the plasmin based cascade which is involved in fibrotic disorders of the vascular system and several organs such as skin , liver , lung and kidney ."
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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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"XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR - XREF_BIBR In this regard TGF-beta1 mediated synthesis and subsequent secretion of PAI-1 can modulate secondary signaling events (ERK or Akt activation) that prevent endothelial cell apoptosis or induce survival programs that precede and necessary for efficient morphogenesis response Pharmacological blockade of ERK1/2 and EGFR, also virtually eliminates endothelial branching induced by TGF-beta1 in keeping with signaling elements necessary for TGF-beta1 mediated PAI-1 induction and subsequent endothelial morphogenesis."
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"We used esophageal biopsy specimens and plasma samples from control and EoE subjects, primary human esophageal epithelial cells, and EoE fibroblasts in immunohistochemistry, quantitative PCR, and immunoassay experiments to understand the induction of PAI-1 by TGFbeta1, the relationship between PAI-1 and esophageal fibrosis, and the role of PAI-1 in fibrotic gene expression."
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"Our findings support the hypothesis that TGF-beta1 induces PAI-1, which suppresses plasmin and plasmin mediated MMP activity, and provide evidence that PAI-1 may be a novel therapeutic target for preventing adhesions and promoting a scarless, regenerative repair of flexor tendon injuries."
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"Further, PAI-1, which is induced by TGF-beta1 activation of the Alk5 and SMAD2/3 pathway, contributes to vessel stabilization by preventing degradation of the provisional matrix deposited around new vessels and favoring the establishment of new basal lamina, again consistently with our finding that PAI-1 was specifically and robustly induced in the low VEGF conditions, leading to the fastest stabilization."
eidos
"It has been confirmed that TGF-beta1 induces PAI-1 synthesis , and a TGF-beta1 response element has been found in the promoter of the PAI-1 gene ; in addition , multiple lines of evidence have determined that PAI-1 expression might be regulated in connection with several signaling pathways ."
| PMC
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"To further confirm this, we detected the PAI-1 and Smad 7 mRNA level in glioblastoma cells treated with TGF-a1, the data showed that PAI-1 mRNA was increased significantly in four cells treated with TGFb1 for 48h, however Smad7 mRNA was not enhanced as highly and significantly as PAI-1 mRNA."
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"Consequently, expression of tissue factor, urokinase receptor, and PAI-1 mRNA and PAI-1 protein secretion induced by busulfan were significantly reduced by the activin A/TGF-beta 1 inhibitor SB 431542 in ECV304 and primary endothelial cells.Conclusions This is the first report that directly relates busulfan exposure to antifibrinolytic activity by PAI-1 and hypercoagulation possibly mediated by members of the TGF-beta1 family."
sparser
"Interestingly, CAGA is also recognized to mediate binding to Smad3 and Smad4, and are required for TGF- β -induced transcriptional activation of the plasminogen activator inhibitor-1 promoter. xref Later studies have suggested that in addition to the GTCT and AGAC elements, Smad4 is also able to recognize a GC-rich sequence. xref , xref It is important to note that Par-4 promoter sequence is extremely GC-rich."