PUBLICATION

Vascular Injury in the Zebrafish Tail Modulates Blood Flow and Peak Wall Shear Stress to Restore Embryonic Circular Network

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.
ID
ZDB-PUB-220405-9
Date
2022
Source
Frontiers in cardiovascular medicine   9: 841101 (Journal)
Registered Authors
Baek, Kyung, Xu, Xiaolei
Keywords
Notch-ephrinb2 signaling, biophysics, peak wall shear stress, vascular injury and repair, vascular loop formation
MeSH Terms
none
PubMed
35369301 Full text @ Front Cardiovasc Med
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.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping