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Hyperbaric oxygen affects endothelial progenitor cells proliferation in vitro
Author(s) -
Benincasa Julia C.,
de Freitas Filho Luiz H.,
Carneiro Giane D.,
Sielski Micheli S.,
Giorgio Selma,
Werneck Claudio C.,
Vicente Cristina P.
Publication year - 2019
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.11070
Subject(s) - wound healing , enos , angiogenesis , nitric oxide , progenitor cell , reactive oxygen species , microbiology and biotechnology , endothelial progenitor cell , in vitro , cell growth , bone marrow , endothelial stem cell , chemistry , immunology , nitric oxide synthase , pharmacology , biology , cancer research , stem cell , biochemistry , endocrinology
Hyperbaric oxygen is a clinical treatment that contributes to wound healing by increasing fibroblasts proliferation, collagen synthesis, and production of growth factors, inducing angiogenesis and inhibiting antimicrobial activity. It also has been shown that hyperbaric oxygen treatment (HBO), through the activation of nitric oxide synthase promotes an increase in the nitric oxide levels that may improve endothelial progenitor cells (EPC) mobilization from bone marrow to the peripheral blood and stimulates the vessel healing process. However, cellular mechanisms involved in cell proliferation and activation of EPC after HBO treatment remain unknown. Therefore, the present work aimed to analyze the effect of HBO on the proliferation of pre‐treated bone marrow‐derived EPC with TNF‐alpha. Also, we investigated the expression of ICAM and eNOS by immunochemistry, the production of reactive species of oxygen and performed an in vitro wound healing. Although 1h of HBO treatment did not alter the rate of in vitro wound closure or cell proliferation, it increased eNOS expression and decreased ICAM expression and reactive oxygen species production in cells pre‐treated with TNF‐alpha. These results indicate that HBO can decrease the inflammatory response in endothelial cells mediated by TNF‐alpha, and thus, promote vascular recovery after injury.