Effect of Endothelin-1 on Proliferation and Differentiation of Rat Tracheal Epithelial Cells
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- 영문명
- Effect of Endothelin-1 on Proliferation and Differentiation of Rat Tracheal Epithelial Cells
- 발행기관
- 대한생리학회-대한약리학회
- 저자명
- Chang Soo Kim Sae Ock Oh Jae Suk Woo Jin Sup Jung Yong Keun Kim Sang Ho Lee
- 간행물 정보
- 『The Korean Journal of Physiology & Pharmacology』제2권 제6호, 763~770쪽, 전체 8쪽
- 주제분류
- 의약학 > 의학일반
- 파일형태
- 발행일자
- 1998.01.01
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국문 초록
영문 초록
A number of substances involved in the proliferation and differentiation of the tracheobronchial epithelium have been identified. The defects in the control of the proliferation and differentiation of tracheobronchial epithelial cells appear to constitute crucial steps in the transition of normal cells to neoplastic ones. Endothelin-1 is produced by tracheal epithelial cells, and its receptors are present in tracheal epithelial cells. However, the effect of endothelin-1 on the proliferation and differentiation of tracheal epithelial cells has not been clearly elucidated. This study was undertaken to investigate these actions of endothelin-1 in primary cultured cells of rat tracheal epithelia. Endothelin-1 stimulated proliferation of tracheal epithelial cells 1.5-fold when compared with that of control cells. Endothelin-1 increased mitogen-activated protein kinase (MAPK) activity. Herbimycin A, a tyrosine kinase inhibitor, inhibited endothelin-1-induced proliferation of epithelial cells. The treatment of endothelin-1 during the primary culture of tracheal epithelial cells increased AB-PAS-stained cell population and ciliated cell population 6.5 fold and 1.5 fold, respectively, when compared with those in control cells. The responsiveness to carbachol and forskolin in the Cl- secretion was increased 1.7 and 1.9 fold, respectively, in the endothelin-treated epithelial cells. These results indicated that endothelin-1 increases proliferation via MAPK pathway and stimulates differentiation to secretory and ciliated cells in rat tracheal epithelial cells.
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