초록접수 현황
| 17F-136 | 포스터 발표 |
The Damage of Lung Epithelial Type II Cell is Associated with Bleomycin-induced Cell Cycle Arrest.
Soojin Jang, Hanbyeol Lee, Jooyeon Lee, Se Min Ryu, Sung-Min Park, Kyung-Hak Lee, Seong-Joon Cho, Se-Ran Yang
Department of Thoracic and Cardiovascular Surgery, Kangwon National University Hospital, Kangwon National University College of Medicine, Gangwon-do, Republic of Korea
Purpose : Pulmonary fibrosis (PF) is a fibrotic lung disease with progressive restrictive-ventilatory limitation and its declining lung function causes an emerging problem of public health. The pathogenesis of PF involved fibroblast-myofibroblast differentiation, excessive extracellular matrix (ECM) deposition. Lung alveolar type II epithelial (AE II) cells are thought to play a critical role with the secretion of surfactant protein C (SP-C) and differentiation potency of AE II – into alveolar type I – cells after epithelial damage. However, it still remains unknown whether bleomycin induces cell cycle arrest in lung AE II cells. Therefore, we determined whether BLM regulates proliferation in MLE-12, mouse lung AE II cells.
Methods : We treated bleomycin at 1, 2.5, 5, 10ng/ml dose for 24h. we analyzed the MTT assay, DAPI staining, Hoecst 33258 staining, PI staining, and ELISA.
Results : In cell proliferation assay, BLM treatment decreased proliferation. In ELISA assay level of TGF-β, TNF-α, and IL-6 pro-inflammatory cytokines were significantly increased in a dose-dependent manner. In addition, BLM exposure increased mRNA level of p21, cyclin-dependent kinase inhibitor 1, while decreased mRNA level of E-cadherin, epithelial cadherin, in the real-time RT-PCR analysis. Morphologically, the enlarged and flatten nuclei were found in Hoechst 33258 staining, BLM arrested G2/M phase in propidium iodide (PI) staining. Therefore, we demonstrate that BLM-induced PF results in G2/M phase arrest, flat cells in morphology and increased inflammation.
Conclusion : Taken together, these data suggest that a bleomycin-induced cell cycle arrest is associated with loss of alveolar repair function.
Methods : We treated bleomycin at 1, 2.5, 5, 10ng/ml dose for 24h. we analyzed the MTT assay, DAPI staining, Hoecst 33258 staining, PI staining, and ELISA.
Results : In cell proliferation assay, BLM treatment decreased proliferation. In ELISA assay level of TGF-β, TNF-α, and IL-6 pro-inflammatory cytokines were significantly increased in a dose-dependent manner. In addition, BLM exposure increased mRNA level of p21, cyclin-dependent kinase inhibitor 1, while decreased mRNA level of E-cadherin, epithelial cadherin, in the real-time RT-PCR analysis. Morphologically, the enlarged and flatten nuclei were found in Hoechst 33258 staining, BLM arrested G2/M phase in propidium iodide (PI) staining. Therefore, we demonstrate that BLM-induced PF results in G2/M phase arrest, flat cells in morphology and increased inflammation.
Conclusion : Taken together, these data suggest that a bleomycin-induced cell cycle arrest is associated with loss of alveolar repair function.
책임저자: Se-Ran Yang
Department of Thoracic and Cardiovascular Surgery, Kangwon National University Hospital, Kangwon National University College of Medicine, Gangwon-do, Republic of Korea
발표자: Soojin Jang, E-mail : tnwls1926@naver.com