Endothelial growth medium suppresses apoptosis of mesenchymal stem cells in vitro via decrease of miR-29a

Abstract

The administration of mesenchymal stem cells (MSCs) in cases of cardiac ischemia/reperfusion injury (IRI) has been associated with a significant reduction of myocardial cell death and an effective improvement in cardiac function. However, one major limiting factor in MSCs transplantation therapy is the low survival rate of the transplanted cells. The present study aimed to demonstrate that human amnion-derived mesenchymal stem cells (hAMSCs) cultured with endothelial growth medium (EGM-2) exhibited reduced apoptosis when exposed to serum-free and hypoxic conditions; and that the expression of microRNA (miR)-29a decreased significantly. Furthermore, miR-29a knockdown resulted in decreased apoptosis of hAMSCs and increased myeloid cell leukemia (MCL)-1 at the mRNA and protein levels. These results suggested that EGM-2 promoted survival of hAMSCs partly through the regulation of miR-29a and MCL-1 expression levels. These findings may provide a novel understanding of a potential effective therapeutic strategy for cardiac IRI.

Hsa‐miRNA‐29a protects against high glucose‐induced damage in human umbilical vein endothelial cells

“…Studies have shown that the expression of miRNA‐29a decreased significantly in human amniotic mesenchymal stem cells (hAMSCs) exposed to serum‐free and hypoxi, and miRNA‐29a knockdown resulted in decreased apoptosis of hAMSCs by increasing myeloid cell leukemia‐1 (MCL‐1). The mechanism study shows that endothelial growth medium (EGM‐2) promoted the survival of hAMSCs partly through the regulation of miRNA‐29a and MCL‐1 expression levels . These studies show that miRNA‐29a plays a vital role in maintaining the normal functioning of HUVECs under normal and hypoxic environments.…”

“…The mechanism study shows that endothelial growth medium (EGM-2) promoted the survival of hAMSCs partly through the regulation of miRNA-29a and MCL-1 expression levels. 13 These studies show that miRNA-29a plays a vital role in maintaining the normal functioning of HUVECs under normal and hypoxic environments. However, they focused on cell injury caused by hypoxia, which is distinct from endothelial injury caused by HG and also did not involve an HG model in vitro or in vivo.…”

“…Yang et al 11 demonstrated that hypoxia-mimicking reagents upregulate miRNA-29a in human umbilical vein endothelial cells (HUVECs) and blocking miRNA-29a suppresses the proliferation and tube formation of HUVECs. 13 These studies show that miRNA-29a plays a vital role in maintaining the normal functioning of HUVECs under normal and hypoxic environments. Furthermore, in mouse endothelial cells (ECs), transforming growth factor-β (TGF-β) upregulates the transcription of miRNA-29a in a Smad4-dependent way and thus reduces PENT levels, increases the activity of AKT, and promotes the tube formation and migration capacity of endothelial cells.…”