| Literature DB >> 30686582 |
Soumyashree Das1, Andrew B Goldstone2, Hanjay Wang2, Justin Farry2, Gaetano D'Amato1, Michael J Paulsen2, Anahita Eskandari2, Camille E Hironaka2, Ragini Phansalkar3, Bikram Sharma4, Siyeon Rhee1, Elya Ali Shamskhou5, Dritan Agalliu6, Vinicio de Jesus Perez5, Y Joseph Woo7, Kristy Red-Horse8.
Abstract
Collateral arteries are an uncommon vessel subtype that can provide alternate blood flow to preserve tissue following vascular occlusion. Some patients with heart disease develop collateral coronary arteries, and this correlates with increased survival. However, it is not known how these collaterals develop or how to stimulate them. We demonstrate that neonatal mouse hearts use a novel mechanism to build collateral arteries in response to injury. Arterial endothelial cells (ECs) migrated away from arteries along existing capillaries and reassembled into collateral arteries, which we termed "artery reassembly". Artery ECs expressed CXCR4, and following injury, capillary ECs induced its ligand, CXCL12. CXCL12 or CXCR4 deletion impaired collateral artery formation and neonatal heart regeneration. Artery reassembly was nearly absent in adults but was induced by exogenous CXCL12. Thus, understanding neonatal regenerative mechanisms can identify pathways that restore these processes in adults and identify potentially translatable therapeutic strategies for ischemic heart disease.Entities:
Keywords: CXCL12; arterialization; arteriogenesis; collateral arteries; endothelial cells; heart regeneration; myocardial infarction
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Year: 2019 PMID： 30686582 PMCID： PMC6435282 DOI： 10.1016/j.cell.2018.12.023
Source DB: PubMed Journal: Cell ISSN： 0092-8674 Impact factor: 41.582