Inhibition of viability and genetic change in hypoxia-treated lung pericytes

Wook Shin Jong, Kae Young Kim, Woo Lee Young, Woo Jung Jae, Jun Lee Byoung, Jae Yeol Kim, Inho Jo, Won Park In, Whui Choi Byoung

Research output: Contribution to journalArticlepeer-review


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 200μM 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-1α(HIF-1α) 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.

Original languageEnglish
Pages (from-to)37-46
Number of pages10
JournalTuberculosis and Respiratory Diseases
Issue number1
StatePublished - Jul 2004


  • Blood-air barrier
  • HIF-1α
  • Hypoxia
  • Pericytes
  • Smad-2
  • VEGF


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