期刊
CELL BIOCHEMISTRY AND BIOPHYSICS
卷 80, 期 2, 页码 435-442出版社
HUMANA PRESS INC
DOI: 10.1007/s12013-021-01031-7
关键词
Human embryonic stem cell; Zoledronate; Ischemia; Reperfusion; Myocardial infarction; Reoxygenation
This study investigated the functions of bisphosphonate of zoledronate (Zd) in hypoxia/reoxygenation (H/R) injured human embryonic stem cell-derived cardiomyocytes (hES-CMs). The results showed that low and medium concentrations of Zd did not induce cell death and could protect against H/R-induced apoptosis. Zd also promoted the survival of hES-CMs in an animal model of myocardial infarction.
In this work, we investigated the in vitro and in vivo functions of bisphosphonate of zoledronate (Zd) in hypoxia/reoxygenation (H/R) injured human embryonic stem cell-derived cardiomyocytes (hES-CMs). In the in vitro setting, the effects of Zd on hES-CM survival and differentiation were examined. We found that low and medium concentrations (<2 mu m) of Zd did not induce cell death of hES-CMs. 0.5 mu m Zd protected H/R-induced hES-CM apoptosis but did not affect key differentiation proteins, including hcTnl, PECM-1 Cnx43 and Pan-Cadherin. In addition, Zd-induced TrkA/B phosphorylation and promoted VEGF to counter the apoptotic effect of H/R injury. In the in vivo animal model of myocardial infarction, Zd treatment promoted the survival of hES-CMs by inducing PECAM1 and hcTnl. Thus, we concluded that Zd protected H/R-induced hES-CM apoptosis in vitro and promoted hES-CM survival in vivo. These data may facilitate the development of human embryonic stem cells into clinical applications for patients with ischemic heart disease.
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