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Erythropoietin signal protected human umbilical vein endothelial cells from high glucose‐induced injury
Author(s) -
Yasuda Haruka,
Iwata Yasunori,
Nakajima Satoshi,
Furuichi Kengo,
Miyake Taito,
Sakai Norihiko,
Kitajima Shinji,
Toyama Tadashi,
Shinozaki Yasuyuki,
Sagara Akihiro,
Miyagawa Taro,
Hara Akinori,
Shimizu Miho,
Kamikawa Yasutaka,
Sato Kouichi,
Oshima Megumi,
YonedaNakagawa Shiori,
Kaneko Shuichi,
Wada Takashi
Publication year - 2019
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1111/nep.13518
Subject(s) - erythropoietin , umbilical vein , erythropoietin receptor , medicine , chemokine , inflammation , cytokine , receptor , proinflammatory cytokine , tissue factor , endocrinology , immunology , biology , biochemistry , in vitro , coagulation
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.

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