Exposure to hypoxia causes structural changes in the endothelial cell (EC) monolayer that alter its permeability. There was a report earlier of impairment of nitric oxide (NO) production in endothelium. Intervention of NO in the altered cellular arrangements of actin cytoskeleton in endothelium for rectification of paracellular gaps in endothelium under hypoxia was observed. The present study demonstrates hypoxia inducing paracellular gaps in hypoxia exposed blood capillaries in chick embryo extra vascular model. Phalloidin staining confirmed significant polymerization of actin and unique cellular localization of the F-actin bands under hypoxia treatments. Addition of spermine NONOate (SPNO), a NO donor, or reoxygenation to endothelial monolayer attenuated hypoxia-mediated effects on endothelial permeability with partial recovery of endothelial integrity through actin remodeling. The present study indicates link of hypoxia-induced actin-associated cytoskeletal rearrangements and paracellular gaps in the endothelium with a low NO availability in the hypoxia milieu. The author concludes that NO confers protection against hypoxia-mediated cytoskeletal remodeling and endothelial leakiness.
Bibliographical note© 2017, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
Funding: Grant (#DLS/81/48201/XI/FYP/DIP- 251/1496/D(R&D) “Human Performance Enhancement Under Different operational Environments” from Defence Institute of Physiology and Allied Science (DIPAS), DRDO, Government of India. This work was partially supported by a grant from the University Grant Commission-Faculty Research Program (UGC-FRP), Government of India to SC
- Actin filaments
- Gap junction
- Nitric Oxide