Details

Autor(en) / Beteiligte

• Liu Weiwei
• Yan, Wang
• Jiao, Li
• Weiyu, Han
• Ranzun, Zhao
• Bei, Shi

Titel

HMGB1 May Modulates Proliferation and Migration of Endothelial Cells by YAP1 under Hypoxia

Ist Teil von

• Biology bulletin of the Russian Academy of Sciences, 2024-04, Vol.51 (2), p.233-242

Ort / Verlag

Moscow: Pleiades Publishing

Erscheinungsjahr

2024

Link zum Volltext

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• Endothelial dysfunction is a key factor in the occurrence of coronary artery disease and plays a vital role in the pathological development of myocardial infarction. Hypoxia contributing to endothelial cell survival and growth, metabolism and angiogenesis. HMGB1 has been identified as one of the factors involved in the regulation of vascular endothelial cell function. However, the mechanisms by which HMGB1 regulates endothelial cells under hypoxia remain unclear. Our study aimed to determine HMGB1 expression investigate the functions of HMGB1 on endothelial cell in hypoxia environment. The expression of extracellular high-mobility group box 1 (HMGB1) in cardiac endothelial cells treated with hypoxia was detected by western blot analysis. 5-Ethynyl-2′-deoxyuridine (EdU) assays and transwell assays were performed to determine the cell proliferation and migration, and flow cytometry assay was performed to evaluate the apoptosis of cardiac endothelial cell. Intracellular HMGB1 expression was upregulated in hypoxia-induced cardiac endothelial cells. HMGB1 silencing significantly promoted apoptosis and inhibited the proliferation and migration of hypoxia-induced cardiac endothelial cells. Moreover, silencing YAP1 on the basis of silencing HMGB1 can aggravate apoptosis and inhibit proliferation and migration of cardiac endothelial cells in hypoxic microenvironment. HMGB1 is up-regulated in hypoxic environment, which may be regulate the biological function of cardiac endothelial cells by YAP1, revealing that HMGB1/YAP1 may be partially involved in the protective mechanism of cardiac endothelial cells. To the best of our knowledge, this study provides a novel basis for the development of treatment methods for ischemic heart diseases.