Ghrelin Boosts Blood Vessel Growth in Human Heart Cells Under Low Oxygen

Angiogenesis, the formation of new blood vessels, is a vital process for tissue repair and regeneration, especially in conditions like ischemic heart disease where oxygen supply is compromised. However, impaired angiogenesis under hypoxia (low oxygen) can significantly worsen patient outcomes and hinder recovery. This study addresses the critical knowledge gap regarding how ghrelin, a hormone known for its metabolic and growth-promoting effects, influences angiogenesis in human coronary artery endothelial cells under hypoxic stress.

The study revealed that ghrelin significantly promoted multiple aspects of angiogenesis in human coronary artery endothelial cells under hypoxic conditions. Treatment with ghrelin at 100 nM led to a robust increase in the cells' ability to form capillary-like structures. Specifically, ghrelin treatment resulted in a 43% increase in total tube formation length and a 38% increase in the number of branch points compared to untreated hypoxic controls (p<0.001). Furthermore, cell proliferation was enhanced by 2.5-fold (p<0.01) and cell migration by 65% (p<0.001) with 100 nM ghrelin. Mechanistically, ghrelin significantly upregulated the expression of VEGF (Vascular Endothelial Growth Factor, a crucial protein for new blood vessel growth) by 3-fold and increased eNOS (endothelial Nitric Oxide Synthase) phosphorylation by 2.8-fold (p<0.001), indicating activation of key pro-angiogenic signaling pathways.