Erythropoietin signal protected human umbilical vein endothelial cells from high glucose‐induced injury

Abstract

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.

The extraction of effective components and an antioxidant activity study of Tulipa edulis

“…However, if the radicals accumulate too much or cannot be removed by antioxidants in the body in a timely manner, then cells and tissues may be damaged, which can lead to a series of diseases [28,29]. ROS can also cause inflammation [16]. Oxidative damage of vascular endothelial cells is closely related to many diseases, such as cardiovascular disease, atherosclerosis and so on [30,31].…”

“…At the same time, the production and accumulation of ROS can mediate the inflammatory response, causing cells to secrete a variety of inflammatory factors, stimulate the immune response and induce apoptosis, thus leading to the occurrence of diseases [13,14]. Studies have shown that high glucose can induce oxidative stress of vascular endothelial cells, and then cause inflammation [15,16]. The damage of vascular endothelial cells is related to many factors, among which oxidative stress is closely related to cardiovascular diseases, atherosclerosis and other diseases [17].…”

Study of the Pharmacological Activity of Novel Epor/Cd131 Heteroreceptor Agonists in Mice With Endothelial-Specific Expression of Mutant Polg Gene

“…В этом же исследовании сообщается, что эритропоэтин опосредованная активация eNOS связана с передачей сигналов PI3K, а связанное с ЭПО снижение проявлений ишемии кардиомиоцитов не наблюдается у мышей с генотипом eNOS -/- [23]. Предполагается, что эритропоэтин индуцированная продукция оксида азота эндотелиоцитами опосредуется, в первую очередь индукцией и активацией eNOS, особенно при пониженном содержании кислорода [24,25]. Кроме того, у мышей с эктопической трансгенной экспрессией ЭПО обнаружена повышенная активность eNOS и повышенный уровень NO в плазме, что предотвращает сердечно-сосудистые заболевания, такие как гипертония и тромбоэмболия, а ингибирование NO-синтазы приводит к сердечно-сосудистой патологии и смерти [3].…”