Abstract:
:Hypoxic preconditioning is a well-known strategy to improve the survival and therapeutic potential of stem cells against various challenges including hemodynamic and neurohormonal modulations. However, the mechanism involved in hypoxia-induced benefits on stem cells is still ambiguous. In pathological hypertension, the elevation of the neurohormonal mediator Angiotensin II (Ang II) causes the adverse effects to stem cells. In this study, we investigate the effect and mechanism of action of short term hypoxia-inducible miRNA in suppressing the effects of AngII on stem cells. According to the results obtained, Ang II affects the normal cell cycle and triggers apoptosis in rADSCs with a corresponding increase in the expression of cell death-inducing p53 target 1 (CDIP1) protein. However, the short term hypoxia-inducible miRNA-miR-210-3p was found to target CDIP1 and reduce their levels upon the Ang II challenge. CDIP1 induces stress-mediated apoptosis involving the extrinsic apoptosis pathway via Bid/Bax/cleaved caspase3 activation. Administration of mimic miR-210-3p targets CDIP1 mRNA by binding to the 3' UTR region as confirmed by dual luciferase assay and also reduced Ang II-induced mitochondrial ROS accumulation as analyzed by MitoSOX staining. Moreover, the present study demonstrates the mechanism of miR-210-3p in the regulation of Ang II-induced CDIP1-associated apoptotic pathway in rADSCs.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Lai CH,Barik P,Hsieh DJ,Day CH,Ho TJ,Chen RJ,Kuo WW,Padma VV,Shibu MA,Huang CYdoi
10.1016/j.bbrc.2020.07.052subject
Has Abstractpub_date
2020-11-12 00:00:00pages
347-354issue
3eissn
0006-291Xissn
1090-2104pii
S0006-291X(20)31441-8journal_volume
532pub_type
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