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OGR1 mediates the inhibitory effects of acidic environment on proliferation and angiogenesis of endothelial progenitor cells
Author(s) -
Ding Shenglong,
Xu Ji,
Zhang Qichen,
Chen Fangyi,
Zhang Jihong,
Gui Keke,
Xiong Min,
Li Bing,
Ruan Zhiyong,
Zhao Mingdong
Publication year - 2019
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.11179
Subject(s) - angiogenesis , progenitor cell , gene silencing , biology , cell growth , small interfering rna , cell migration , microbiology and biotechnology , endothelial stem cell , cell cycle , endothelial progenitor cell , apoptosis , cell , cell culture , chemistry , cancer research , stem cell , biochemistry , in vitro , transfection , genetics , gene
Ovarian cancer G‐protein‐coupled receptor 1 (OGR1), an acid‐sensitive receptor, plays a key proton‐sensing role through stimulation of inositol phosphate formation. Avascular necrosis of the femoral head is characterized by apoptosis of bone cells mainly resulting from deficient local blood perfusion, eventually leading to acidification with disruption of endothelial progenitor cells’ (EPCs) function. However, whether EPCs express OGR1 has not been demonstrated. This study attempted to whether OGR1 mediates the effects of acid on proliferation, migration, and angiogenesis in EPCs. FITC‐UEA‐I and Dil‐Ac‐LDL double‐staining methods were used to identify EPCs. Expression of OGR1 was analyzed by RT‐PCR (reverse transcription PCR) and western blot after incubation in media ranging in pH, cell counting kit‐8 and cell cycle analysis were used to analyze proliferation and cell cycle distribution. Scratch test, transwell migration assay, and tube formation experiments were performed to analyze migration and vascularization of EPCs after silencing OGR1 with small interfering RNA (siRNA). The result show EPCs were positive for FITC‐UEA‐I and Dil‐Ac‐LDL double‐staining and expressed OGR1. The expression of OGR1 increased gradually with decreased pH and was highest in pH 6.4 medium. Incubation in pH 6.4 medium inhibited proliferation of EPCs and caused cell cycle arrest. Silencing of OGR1 using siRNA partially reversed the effect of acidic environment on EPCs. Migration and angiogenesis of EPCs were inhibited in pH 6.4 medium, and silencing of OGR1 partially reversed this effect. The results demonstrated expression of OGR1 in EPCs, and the OGR1 mediated the effects of acidic environment on proliferation, migration, and angiogenesis of EPCs.