PUBLICATION

Dissecting VEGF-induced acute versus chronic vascular hyperpermeability: Essential roles of dimethylarginine dimethylaminohydrolase-1

Authors
Wang, Y., Angom, R.S., Kulkarni, T.A., Hoeppner, L.H., Pal, K., Wang, E., Tam, A., Valiunas, R.A., Dutta, S.K., Ji, B., Jarzebska, N., Chen, Y., Rodionov, R.N., Mukhopadhyay, D.
ID
ZDB-PUB-211028-3
Date
2021
Source
iScience   24: 103189 (Journal)
Registered Authors
Angom, Ramcharan Singh, Dutta, Shamit, Mukhopadhyay, Debabrata, Wang, Enfeng, Wang, Ying
Keywords
Cardiovascular medicine, Molecular genetics
MeSH Terms
none
PubMed
34703990 Full text @ iScience
Abstract
Vascular endothelial cell growth factor (VEGF) is a key regulator of vascular permeability. Herein we aim to understand how acute and chronic exposures of VEGF induce different levels of vascular permeability. We demonstrate that chronic VEGF exposure leads to decreased phosphorylation of VEGFR2 and c-Src as well as steady increases of nitric oxide (NO) as compared to that of acute exposure. Utilizing heat-inducible VEGF transgenic zebrafish (Danio rerio) and establishing an algorithm incorporating segmentation techniques for quantification, we monitored acute and chronic VEGF-induced vascular hyperpermeability in real time. Importantly, dimethylarginine dimethylaminohydrolase-1 (DDAH1), an enzyme essential for NO generation, was shown to play essential roles in both acute and chronic vascular permeability in cultured human cells, zebrafish model, and Miles assay. Taken together, our data reveal acute and chronic VEGF exposures induce divergent signaling pathways and identify DDAH1 as a critical player and potentially a therapeutic target of vascular hyperpermeability-mediated pathogenesis.
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