Vascular injury in the zebrafish tail modulates blood flow and peak wall shear stress to restore embryonic circular network Journal Article


Authors: Baek, K. I.; Chang, S. S.; Chang, C. C.; Roustaei, M.; Ding, Y.; Wang, Y.; Chen, J.; O'Donnell, R.; Chen, H.; Ashby, J. W.; Xu, X.; Mack, J. J.; Cavallero, S.; Roper, M.; Hsiai, T. K.
Article Title: Vascular injury in the zebrafish tail modulates blood flow and peak wall shear stress to restore embryonic circular network
Abstract: Mechano-responsive signaling pathways enable blood vessels within a connected network to structurally adapt to partition of blood flow between organ systems. Wall shear stress (WSS) modulates endothelial cell proliferation and arteriovenous specification. Here, we study vascular regeneration in a zebrafish model by using tail amputation to disrupt the embryonic circulatory loop (ECL) at 3 days post fertilization (dpf). We observed a local increase in blood flow and peak WSS in the Segmental Artery (SeA) immediately adjacent to the amputation site. By manipulating blood flow and WSS via changes in blood viscosity and myocardial contractility, we show that the angiogenic Notch-ephrinb2 cascade is hemodynamically activated in the SeA to guide arteriogenesis and network reconnection. Taken together, ECL amputation induces changes in microvascular topology to partition blood flow and increase WSS-mediated Notch-ephrinb2 pathway, promoting new vascular arterial loop formation and restoring microcirculation.
Keywords: angiogenesis; vascular; eph receptors; biophysics; expression; cell-proliferation; notch; endothelial-cells; fate; arterial; ephrin-b2; peak wall shear stress; notch-ephrinb2 signaling; loop formation; vascular injury and repair; venous vessels
Journal Title: Frontiers in Cardiovascular Medicine
Volume: 9
ISSN: 2297-055X
Publisher: Frontiers Media S.A.  
Date Published: 2022-03-18
Start Page: 841101
Language: English
ACCESSION: WOS:000808435100001
DOI: 10.3389/fcvm.2022.841101
PROVIDER: wos
PMCID: PMC8971683
PUBMED: 35369301
Notes: Article -- Source: Wos
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  1. Shyr-Shea Chang
    1 Chang