TLR4 signaling promotes the expression of VEGF and TGFβ1 in human prostate epithelial PC3 cells induced by lipopolysaccharide

Pei, Zengyang; Lin, Dazhen; Song, Xiaoyu; Li, Hui; Yao, Hairui

doi:10.1016/j.cellimm.2008.06.007

Cited by 49 publications

(45 citation statements)

References 47 publications

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“…The effect of endotoxin in increasing the expression of TGF-␤1 and TGF-␤2 was mediated through its receptor, TLR-4. These findings were in agreement with those observed in a cell line derived from human prostate epithelial cells, in which endotoxin exposure induces TGF-␤1 expression (20). Furthermore, the activation of NAD(P)H oxidase and the subsequent generation of ROS were crucial for the increase of endotoxin-induced TGF-␤1 and TGF-␤2 expression.…”

Section: Discussionsupporting

confidence: 81%

Endotoxin-Induced Endothelial Fibrosis Is Dependent on Expression of Transforming Growth Factors β1 and β2

et al. 2014

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f During endotoxemia-induced inflammatory disease, bacterial endotoxins circulate in the bloodstream and interact with endothelial cells (ECs), inducing dysfunction of the ECs. We previously reported that endotoxins induce the conversion of ECs into activated fibroblasts. Through endotoxin-induced endothelial fibrosis, ECs change their morphology and their protein expression pattern, thereby suppressing endothelial markers and upregulating fibrotic proteins. The most commonly used fibrotic inducers are transforming growth factor ␤1 (TGF-␤1) and TGF-␤2. However, whether TGF-␤1 and TGF-␤2 participate in endotoxin-induced endothelial fibrosis remains unknown. We have shown that the endotoxin-induced endothelial fibrosis process is dependent on the TGF-␤ receptor, ALK5, and the activation of Smad3, a protein that is activated by ALK5 activation, thus suggesting that endotoxin elicits TGF-␤ production to mediate endotoxin-induced endothelial fibrosis. Therefore, we investigated the dependence of endotoxin-induced endothelial fibrosis on the expression of TGF-␤1 and TGF-␤2. Endotoxin-treated ECs induced the expression and secretion of TGF-␤1 and TGF-␤2. TGF-␤1 and TGF-␤2 downregulation inhibited the endotoxininduced changes in the endothelial marker VE-cadherin and in the fibrotic proteins ␣-SMA and fibronectin. Thus, endotoxin induces the production of TGF-␤1 and TGF-␤2 as a mechanism to promote endotoxin-induced endothelial fibrosis. To the best of our knowledge, this is the first report showing that endotoxin induces endothelial fibrosis via TGF-␤ secretion, which represents an emerging source of vascular dysfunction. These findings contribute to understanding the molecular mechanism of endotoxin-induced endothelial fibrosis, which could be useful in the treatment of inflammatory diseases.

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Section: Discussionsupporting

confidence: 81%

Endotoxin-Induced Endothelial Fibrosis Is Dependent on Expression of Transforming Growth Factors β1 and β2

et al. 2014

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“…26 Several previous reports have shown that LPS stimulation can up-regulate TLR4 expression in various epithelial cells. 27 Consistent with these results, LPS induced TLR4 expression in PCK cholangiocytes in vitro, and immunohistochemical analysis showed that TLR4 was upregulated in the biliary epithelium of the PCK rats. Thus, modulation of the signaling pathways through up-regulation of TLR4 may contribute to biliary pathogenesis of PCK rats.…”

Section: Discussionsupporting

confidence: 73%

Biliary Infection May Exacerbate Biliary Cystogenesis Through the Induction of VEGF in Cholangiocytes of the Polycystic Kidney (PCK) Rat

Ren

Sato

Harada

et al. 2011

The American Journal of Pathology

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Cholangitis arising from biliary infection dominates the prognosis in Caroli's disease. To clarify the influences of bacterial infection on the biliary cystogenesis, in vivo and in vitro studies were performed using the polycystic kidney (PCK) rat as an animal model of Caroli's disease. Cholangitis became a frequent histological finding in aged PCK rats, and neovascularization around the bile ducts also increased in aged PCK rats. Immunohistochemistry revealed that expression of vascular endothelial growth factor (VEGF) was increased in PCK rat biliary epithelium.

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“…LPS-induced inflammatory responses have been shown to regulate cancer development/ progression in several ways: (i) they may potentiate expression of proteins involved in the breakdown of the extracellular matrix (47); (ii) increase adhesive properties of cancer cells that are essential for the metastatic colonization of a normal tissue (25); (iii) induce recruitment of inflammatory cells into the tumor microenvironment, which in turn can contribute to extracellular matrix turnover (48); (iv) regulate angiogenesis (49); and (v) modulate, as indicated by our study, the cell surface-associated proteolysis by triggering PLG receptor exteriorization. LPS-triggered ENO-1 translocation was found to be independent of the classical endoplasmic reticulum-Golgi pathway and de novo protein synthesis, and it was associated with increased levels of Ca 2ϩ .…”

Section: Discussionmentioning

confidence: 99%

STIM1/ORAI1-mediated Ca2+ Influx Regulates Enolase-1 Exteriorization

Didiášová

Zakrzewicz

Magdolen

et al. 2015

Journal of Biological Chemistry

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Background: Cell surface-associated enolase-1 regulates plasmin formation and thus pericellular proteolysis. Results: STIM1/ORAI1-mediated Ca 2ϩ influx controls enolase-1 exteriorization in cancer cells. Conclusion: Extracellular enolase-1 regulates migratory and invasive properties of cancer cells. Significance: Enhanced exteriorization of enolase-1 may aggravate the malignant behavior of cancer cells and thus contribute to metastasis formation.

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TLR4 signaling promotes the expression of VEGF and TGFβ1 in human prostate epithelial PC3 cells induced by lipopolysaccharide

Cited by 49 publications

References 47 publications

Endotoxin-Induced Endothelial Fibrosis Is Dependent on Expression of Transforming Growth Factors β1 and β2

Endotoxin-Induced Endothelial Fibrosis Is Dependent on Expression of Transforming Growth Factors β1 and β2

Biliary Infection May Exacerbate Biliary Cystogenesis Through the Induction of VEGF in Cholangiocytes of the Polycystic Kidney (PCK) Rat

STIM1/ORAI1-mediated Ca2+ Influx Regulates Enolase-1 Exteriorization

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