Erythropoietin signal protected HUVEC from high glucose induced injury.
Authors of this article are:
Yasuda H, Iwata Y, Nakajima S, Furuichi K, Miyake T, Sakai N, Kitajima S, Toyama T, Shinozaki Y, Sagara A, Miyagawa T, Hara A, Shimizu M, Kamikawa Y, Sato K, Oshima M, Yoneda-Nakagawa S, Kaneko S, Wada T.
A summary of the article is shown below:
AIM: High glucose (HG) induces endothelial injury in vasculature, leading to tissue injury in diabetic condition. Therefore, diabetes is one of the major cause of end stage kidney disease as well as cardiovascular diseases. Chronic inflammation is involved in the progression of HG induced cell injury. Recently, it has been reported that erythropoietin (EPO) protects the tissues from some kind of injury, such as hypoxia and mechanical stress. However, the contribution of EPO to HG induced tissue injury remains to be explored. Therefore, we hypothesized that EPO protects endothelial cells from HG induced injury via the regulation of inflammatory and anti-inflammatory balance.METHODS: We performed genome-wide transcriptome profiling in human umbilical vein endothelial cells (HUVEC), which were stimulated by HG with/without EPO treatment and detected the expression of inflammation associated genes.RESULTS: The expression pattern of mRNA expression in HG stimulated HUVEC with/without EPO were different in hieralchial clustering analysis. While inflammatory cytokines/chemokines mRNA expression were increased by the HG stimulation in HUVEC, Th2 related cytokine receptors and intracellular signaling molecules showed the reduced mRNA expression levels. EPO treatment reduced inflammatory cytokines/chemokines mRNA expression and increased Th2 related cytokine mRNA expression levels. Moreover, EPO stimulation increased mRNA expression of EPO receptor and β-common receptor.CONCLUSION: EPO signaling protects HG induced cell injury by the regulation of immune balance. This article is protected by copyright. All rights reserved.This article is protected by copyright. All rights reserved.
Check out the article’s website on Pubmed for more information:
This article is a good source of information and a good way to become familiar with topics such as:
Categories: Science News