Sodium selenite inhibits the expression of VEGF, TGFβ1 and IL-6 induced by LPS in human PC3 cells via TLR4-NF-KB signaling blockage

Pei, Zengyang; Li, Hui; Guo, Ying; Jin, Yipeng; Lin, Dazhen

doi:10.1016/j.intimp.2009.09.020

Cited by 62 publications

(42 citation statements)

References 45 publications

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“…Moreover, in our study, an increase in serum levels of IL-6 levels was significantly lower in the selenium group than placebo. By regulating the expression of selenoprotein genes, selenium has been shown to inhibit the activation of nuclear factor kappa B (NF-κB) signaling pathway and therefore decrease the production of inflammatory cytokines such as IL-6 [33,34]. Therefore, based on the findings of our study, the observed beneficial effect of selenium supplementation on improving the nutritional status of HD patients may be partly mediated by the inhibition of oxidative damage and inflammation.…”

Section: Discussionmentioning

confidence: 54%

Selenium supplementation improves the nutritional status of hemodialysis patients: a randomized, double-blind, placebo-controlled trial

Salehi

Sohrabi

Ekramzadeh

et al. 2012

Nephrology Dialysis Transplantation

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Section: Discussionmentioning

confidence: 54%

Selenium supplementation improves the nutritional status of hemodialysis patients: a randomized, double-blind, placebo-controlled trial

Salehi

Sohrabi

Ekramzadeh

et al. 2012

Nephrology Dialysis Transplantation

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“…56,57 Recently, Biscetti 58 has reported that HMGB1 promotes angiogenesis through VEGF-dependent mechanism in peripheral ischemia model in diabetic mice. A significant reduction in HMGB1-induced angiogenesis was observed when VEGF activity was suppressed.…”

Section: Discussionmentioning

confidence: 99%

Angiogenesis Mediated by Toll-Like Receptor 4 in Ischemic Neural Tissue

Sun

Ren

Lin

et al. 2013

ATVB

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Objective-Activation of the immune system via toll-like receptors (TLRs) is implicated in atherosclerosis, microvascular complications, and angiogenesis. However, the involvement of TLRs in inflammation-associated angiogenesis in ischemic neural tissue has not been investigated. The goal of this study is to determine the role of TLR4 signaling in oxygeninduced neovascularization in retina, a neural tissue. Methods and Results-In oxygen-induced retinopathy model, we found that retinal neovascularization was significantly attenuated in TLR4 −/− mice. The further study revealed that the absence of TLR4 led to downregulation of proinflammatory factors in association with the attenuated activation of glia in the ischemic retina, which was also associated with reduced expression of high-mobility group box-1, an endogenous ligand for TLR4. The application of high-mobility group box-1 to the ischemic retina promoted the production of proinflammatory factors in wild-type but not TLR4 −/− mice. Highmobility group box-1 treatment in vitro also significantly promoted the production of proinflammatory factors in retinal glial cells from wild-type mice, but much less from TLR4 −/− mice. Conclusion-Our results suggest that the release of high-mobility group box-1 in ischemic neural tissue initiates TLR4-dependent responses that contribute to neovascularization. These findings represented a previously unrecognized effect of TLR4 on angiogenesis in association with the activation of glia in ischemic neural tissue.

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“…Because LPS induces the expression of VEGF through the TLR4-NF-B signaling pathway in certain types of cells, 21,22 we examined the involvement of the signaling pathway in the induction of VEGF in cholangiocytes. As expected, LPS induced the activation of NF-B in cholangiocytes.…”

Section: Discussionmentioning

confidence: 99%

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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Sodium selenite inhibits the expression of VEGF, TGFβ1 and IL-6 induced by LPS in human PC3 cells via TLR4-NF-KB signaling blockage

Cited by 62 publications

References 45 publications

Selenium supplementation improves the nutritional status of hemodialysis patients: a randomized, double-blind, placebo-controlled trial

Selenium supplementation improves the nutritional status of hemodialysis patients: a randomized, double-blind, placebo-controlled trial

Angiogenesis Mediated by Toll-Like Receptor 4 in Ischemic Neural Tissue

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

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