Role of Mydgf in the regulation of hypoxia/reoxygenation-induced apoptosis in cardiac microvascular endothelial cells.

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Date: Sept. 2022
Publisher: Springer
Document Type: Report; Brief article
Length: 275 words

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Abstract :

Keywords: Myeloid-derived growth factor; Cardiac microvascular endothelial cells; Hypoxia/reoxygenation; Apoptosis; Endoplasmic reticulum stress Abstract We aimed to explore the effects of myeloid-derived growth factor (Mydgf) on the regulation of hypoxia/reoxygenation (HR)--induced apoptosis of cardiac microvascular endothelial cells (CMECs). CMECs were exposed to hypoxia for 24 h and reoxygenation for 6 h to establish an HR cell model. Subsequently, an adenovirus was used to overexpress Mydgf in CMECs. Flow cytometry and TUNEL staining were used to detect the extent of apoptosis, whereas qPCR was used to detect the relative expression of Mydgf mRNA. Western blotting was also performed to detect the expression of apoptosis-related proteins and endoplasmic reticulum stress (ERS)--related proteins, including C/EBP Homologous Protein (CHOP), glucose-regulated protein 78 (GRP 78), and cleaved Caspase-12. The endoplasmic reticulum stress agonist tunicamycin (TM) was used to stimulate CMECs for 24 h as a rescue experiment for Mydgf. Flow cytometry revealed that the HR model effectively induced endothelial cell apoptosis, whereas qPCR and western blotting showed that Mydgf mRNA and protein levels decreased significantly after HR treatment (P Author Affiliation: (1) Department of Cardiology, Affiliated Hospital of Zunyi Medical University, 563000, Zunyi, China (j) Article History: Registration Date: 07/13/2022 Received Date: 02/22/2022 Accepted Date: 06/23/2022 Online Date: 08/25/2022 Byline:

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Gale Document Number: GALE|A721886632