Dynamic expression of CyclinD1 and p21CIP1 during lung development in rats
ZHU Hua-Ping, CHANG Li-Wen, LI Wen-Bin
Department of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Email: lwchang@tjh.tjmu.edu.cn
Abstract OBJECTIVE: CyclinD1 and p21CIP1 are major proteins to regulate lung cell proliferation and involved in lung development and lung injury reparation. This study aimed to explore the expression manners of CyclinD1 and p21CIP1 at canalicular, saccular and alveolar stages during lung development in Sprague-Dawley rats. METHODS: Lung tissues were obtained from fetal rats of 20 and 21 days gestational ages, and neonatal rats at 0, 3, 7, 14 and 21 days (n=6). Lung tissues were used for histopathology and the protein analysis of CyclinD1 and p21CIP1 (immunohistochemistry and Western blot). RESULTS: The strongest expression of CyclinD1 and the weakest expression of p21CIP1 occurred at 20-21 days gestation (canalicular stage). At the canalicular stage, CyclinD1 was mainly expressed in epithelial cells, and the expression of p21CIP1was negative. At the saccular stage, the expression of CyclinD1 decreased significantly and the p21CIP1 expression increased significantly. Positive expression of CyclinD1 and p21CIP1 was found in epithelial cells and interstitial cells. At the alveolar stage, the CyclinD1 expression was the lowest and the p21CIP1 expression was the highest. The positive expression of CyclinD1 was found in interstitial cells and that of p21CIP1 was found in epithelial cells. CONCLUSIONS: The location and quantity of CyclinD1 and p21CIP1 expression are different at various stages during lung development in rats. A strongest CyclinD1 expression found in the canalicular stage may be associated a high lung cell proliferation. A strongest p21CIP1 expression found in the alveolar stage may be associated with alveolar maturity.
［5］Duli'c V, Kaufmann WK, Wilson SJ, Tlsty TD, Lees E, Harper JW, et al. P53-dependent inhibition of cyclin-dependent kinase activities in human fibroblasts during radiationinduced G1 arrest［J］. Cell, 1994, 76(5):1013-1023.
［6］Cayrol C, Ducommun B. Interaction with cyclin-dependent kinases and PCNA modulates proteasome-dependent degradation of p21［J］.Oncogene,1998,17(19): 2437-2444.
［7］Luyet C, Burri PH, Schittny JC. Suppression of cell proliferation and programmed cell death by dexamethasone during postnatal lung development［J］. Am J Physiol Lung Cell Mol Physiol, 2002, 282(3): L477-L483.
［8］O'Reilly MA, Watkins RH, Staversky RJ, Maniscalco WM. Induced p21Cip1 in premature baboons with CLD: implications for alveolar hypoplasia［J］. Am J Physiol Lung Cell Mol Physiol, 2003,285(4):L964-L971.
