Hypoxia perturbs endothelium by re-organizing cellular actin architecture: Nitric oxide offers limited protection

Akila Swaminathan; Dharanibalan Kasiviswanathan; Uma Maheswari Balaguru; Gopi Kolluru; Geetha Suryakumar; Suvro Chattejee

doi:10.1016/j.tice.2017.12.007

Hypoxia perturbs endothelium by re-organizing cellular actin architecture: Nitric oxide offers limited protection

Akila Swaminathan, Dharanibalan Kasiviswanathan, Uma Maheswari Balaguru, Gopi Kolluru, Geetha Suryakumar, Suvro Chattejee

Aston Medical School

Research output: Contribution to journal › Article › peer-review

Abstract

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.

Original language	English
Pages (from-to)	114-124
Number of pages	11
Journal	Tissue and Cell
Volume	50
Early online date	23 Dec 2017
DOIs	https://doi.org/10.1016/j.tice.2017.12.007
Publication status	Published - 1 Feb 2018

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

Keywords

Actin filaments
Endothelium
Gap junction
Hypoxia
Nitric Oxide
Permeability

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10.1016/j.tice.2017.12.007

Hypoxia perturbs endothelium by re-organizing cellular actin architecture - Nitric oxide offers limited protection
© 2017, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
Accepted author manuscript, 1.3 MB

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title = "Hypoxia perturbs endothelium by re-organizing cellular actin architecture: Nitric oxide offers limited protection",

abstract = "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.",

keywords = "Actin filaments, Endothelium, Gap junction, Hypoxia, Nitric Oxide, Permeability",

author = "Akila Swaminathan and Dharanibalan Kasiviswanathan and Balaguru, {Uma Maheswari} and Gopi Kolluru and Geetha Suryakumar and Suvro Chattejee",

note = "{\textcopyright} 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",

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AU - Suryakumar, Geetha

AU - Chattejee, Suvro

N1 - © 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

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N2 - 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.

AB - 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.

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KW - Gap junction

KW - Hypoxia

KW - Nitric Oxide

KW - Permeability

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ER -

Hypoxia perturbs endothelium by re-organizing cellular actin architecture: Nitric oxide offers limited protection

Abstract

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Keywords

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