Hyperbaric oxygen affects endothelial progenitor cells proliferation in vitro

被引:21
作者
Benincasa, Julia C. [1 ]
de Freitas Filho, Luiz H. [1 ]
Carneiro, Giane D. [1 ]
Sielski, Micheli S. [1 ]
Giorgio, Selma [2 ]
Werneck, Claudio C. [3 ]
Vicente, Cristina P. [1 ]
机构
[1] State Univ Campinas UNICAMP, Dept Struct & Funct Biol, Sao Paulo, Brazil
[2] Univ Estadual Campinas, Dept Anim Biol, BR-13083865 Campinas, Brazil
[3] State Univ Campinas UNICAMP, Inst Biol, Dept Biochem & Tissue Biol, Sao Paulo, Brazil
基金
巴西圣保罗研究基金会;
关键词
cell therapy; endothelial progenitor cell; hyperbaric oxygen; inflammation; tumor necrosis factor-alpha; wound healing; NECROSIS-FACTOR-ALPHA; NITRIC-OXIDE; STEM; MOBILIZATION; HYPEROXIA; THERAPY; SULFATE; INJURY;
D O I
10.1002/cbin.11070
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:136 / 146
页数:11
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