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Inhibition of Viability and Genetic Change in Hypoxia-treated Lung Pericytes  

Shin, Jong Wook (Department of Internal Medicine, Chung-Ang University School of Medicine)
Kim, Kae-Young (Division of Cardiovascular Diseases, Institute of Biomedical Research, Korean National Institute of Health)
Lee, Young Woo (Department of Internal Medicine, Chung-Ang University School of Medicine)
Jung, Jae Woo (Department of Internal Medicine, Chung-Ang University School of Medicine)
Lee, Byoung Jun (Department of Internal Medicine, Chung-Ang University School of Medicine)
Kim, Jae-Yeol (Department of Internal Medicine, Chung-Ang University School of Medicine)
Jo, Inho (Division of Cardiovascular Diseases, Institute of Biomedical Research, Korean National Institute of Health)
Park, In Won (Department of Internal Medicine, Chung-Ang University School of Medicine)
Choi, Byoung Whui (Department of Internal Medicine, Chung-Ang University School of Medicine)
Publication Information
Tuberculosis and Respiratory Diseases / v.57, no.1, 2004 , pp. 37-46 More about this Journal
Abstract
Background : Lung pericytes are important constituent cells of blood-air barrier in pulmonary microvasculature. These cells take part in the control of vascular contractility and permeability. In this study, it was hypothesized that change of lung pericytes might be attributable to pathologic change in microvasculature in acute lung injury. The purpose of this study was how hypoxia change proliferation and genetic expression in lung pericytes. Methods : From the lungs of several Sprague-Dawley rats, performed the primary culture of lung pericytes and subculture. Characteristics of lung pericytes were confirmed with stellate shape in light microscopy and immunocytochemistry. 2% concentration of oxygen and $200{\mu}M$ $CoCl_2$ were treated to cells. Tryphan blue method and reverse transcription-polymerase chain reaction were done. Results : 1. We established methodology for primary culture of lung pericytes. 2. Hypoxia inhibited cellular proliferation in pericytes. 3. Hypoxia could markedly induce vascular endothelial growth factor(VEGF) and smad-2. 4. Hypoxia-inducible factor-$1{\alpha}$(HIF-$1{\alpha}$) was also induced by 2% oxygen. Conclusion : Viability of lung pericytes are inhibited by hypoxia. Hypoxia can stimulate expression of hypoxia-responsive genes. Pericytic change may be contributed to dysfunction of alveolar-capillary barrier in various pulmonary disorders.
Keywords
pericytes; hypoxia; VEGF; Smad-2; HIF-$1{\alpha}$; blood-air barrier;
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