| Inhibition of Viability and Genetic Change in Hypoxia-treated Lung Pericytes. |
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Jong Wook Shin, Kae Young Kim, Young Woo Lee, Jae Woo Jung, Byoung Jun Lee, Jae Yeol Kim, In Ho Jo, In Won Park, Byoung Whui Choi |
1Department of Internal Medicine, Chung-Ang University School of Medicine, Seoul, Republic of Korea. bwchoimd@nownuri.net
2Division of Cardiovascular Diseases, Institute of Biomedical Research, Korean National Institute of Health, Seoul, Republic of Korea. |
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| 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 200muM CoCl2 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-1alpha (HIF-1alpha)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. |
| Key Words:
pericytes, hypoxia, VEGF, Smad-2, HIF-1alpha, blood-air barrier |
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