A Unique Collateral Artery Development Program Promotes Neonatal Heart Regeneration | Zendy

Soumyashree Das | Zendy; Andrew B. Goldstone | Zendy; Hanjay Wang | Zendy; Justin M. Farry | Zendy; Gaetano D’Amato | Zendy; Michael J. Paulsen | Zendy; Anahita Eskandari | Zendy; Camille E. Hironaka | Zendy; Ragini Phansalkar | Zendy; Bikram Sharma | Zendy; Siyeon Rhee | Zendy; Elya A. Shamskhou | Zendy; Dritan Agalliu | Zendy; Vinicio de Jesús Pérez | Zendy; Y. Joseph Woo | Zendy; Kristy RedHorse | Zendy

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A Unique Collateral Artery Development Program Promotes Neonatal Heart Regeneration

Author(s) -

Soumyashree Das,

Andrew B. Goldstone,

Hanjay Wang,

Justin M. Farry,

Gaetano D’Amato,

Michael J. Paulsen,

Anahita Eskandari,

Camille E. Hironaka,

Ragini Phansalkar,

Bikram Sharma,

Siyeon Rhee,

Elya A. Shamskhou,

Dritan Agalliu,

Vinicio de Jesús Pérez,

Y. Joseph Woo,

Kristy RedHorse

Publication year - 2019

Publication title -

cell

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 26.304

H-Index - 776

eISSN - 1097-4172

pISSN - 0092-8674

DOI - 10.1016/j.cell.2018.12.023

Subject(s) - artery , biology , regeneration (biology) , coronary arteries , medicine , collateral circulation , arteriogenesis , cardiology , heart disease , collateral , ischemia , microbiology and biotechnology , finance , economics

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.

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