Key result
Ghrelin inhibits hypoxia-induced increases in myocardial angiogenesis, miR-210, HIF-1α, and VEGF in rats.
Why the study?
Hypoxia stimulates angiogenesis involving HIF-1α, VEGF, and miR-210, but the effects of hypoxia and/or ghrelin on these cardiac markers remained to be examined.
Does ghrelin reduce hypoxia-induced cardiac angiogenesis and associated signalling pathways in rats?
Does ghrelin reduce hypoxia-induced cardiac angiogenesis and associated signalling pathways in rats?
Ghrelin inhibits hypoxia-induced cardiac angiogenesis and downregulates the miR-210/HIF-1α/VEGF pathway in a rat model, suggesting potential anti-angiogenic properties.
Answers are grounded in this paper and cite their sources.
Should not change clinical practice; leaves open ghrelin’s role in hypoxia-related cardiac angiogenesis for future translational research.
OBJECTIVE: Hypoxia is the main stimulus for angiogenesis. Hypoxia-inducible factor (HIF)-1α, vascular endothelial growth factor (VEGF), and miR-210 are involved in the hypoxia-induced angiogenesis. This study examined the effects of hypoxia and/or ghrelin on miR-210, HIF-1α, and VEGF levels in the heart of rats. METHODS: = 6): control; ghrelin, received daily intraperitoneal injections of ghrelin; hypoxia, was exposed to hypoxic condition; hypoxia + ghrelin, was exposed to hypoxic condition and received intraperitoneal injections of ghrelin, for 2 weeks. Myocardial angiogenesis, the expression level of miR-210, and protein levels of HIF-1α and VEGF were assayed in the heart samples. RESULTS: Hypoxia increased myocardial angiogenesis and cardiac levels of miR-210, HIF-1α, and VEGF. However, ghrelin inhibited these hypoxia-induced changes. Interestingly, ghrelin had no significant effect on miR-210, HIF-1α, and VEGF levels in normoxic condition. CONCLUSION: Ghrelin may be useful as an anti-angiogenic factor.
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Mirzaei et al. (2019) studied Hypoxia-induced cardiac angiogenesis. Ghrelin vs. Control (normoxia) and hypoxia alone was evaluated on Myocardial angiogenesis and cardiac levels of miR-210, HIF-1α, and VEGF. Ghrelin inhibited hypoxia-induced increases in myocardial angiogenesis and cardiac levels of miR-210, HIF-1α, and VEGF in rats, but had no significant effect under normoxic conditions.
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