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Expression of cyclin‐dependent kinase inhibitors, p21 cip1 and p27 kip1 , during wound healing in rats
Author(s) -
Zhu Xudong,
Hu Chengxiang,
Zhang Yan,
Li Lei,
Wang Zhengguo
Publication year - 2001
Publication title -
wound repair and regeneration
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.847
H-Index - 109
eISSN - 1524-475X
pISSN - 1067-1927
DOI - 10.1046/j.1524-475x.2001.00205.x
Subject(s) - wound healing , cell growth , cell cycle , kinase , microbiology and biotechnology , cyclin , cancer research , cell cycle checkpoint , biology , cyclin dependent kinase , cyclin dependent kinase 2 , chemistry , cell , protein kinase a , immunology , biochemistry
Wound healing is a physiological process in which growth of cells is stringently regulated. Cell growth is controlled by cell cycle‐related proteins in which the cyclin kinase inhibitors cause cell cycle arrest and inhibit proliferation. However, little is known about the expression and the role of cyclin kinase inhibitors during wound healing in vivo. This study was mainly designed to examine the expression of p21 cip1 and p27 kip1 in excisional wounds of full‐thickness skin in rats. Concomitant expression of proliferation marker Ki67 was also examined. Proliferation predominantly occurred in the first week after injury, peaking at postwounding day 5. Expression of both p21 cip1 and p27 kip1 at the gene and protein levels did occur during wound healing and showed an inverse gradient to that of Ki67. Constitutive p27 kip1 was expressed throughout wound healing with low levels during the proliferating period of days 3 and 5 and increased levels during post‐mitotic and remodeling stages. In contrast, p21 cip1 was expressed transiently with detectable levels only between days 7 and 14 by Western blot analysis. Immunohistochemically, epithelial cells, endothelial cells and fibroblasts all could express both p21 cip1 and p27 kip1 . In conclusion, the overall results suggested that p21 cip1 and p27 kip1 may play a key role in supervising the growth resulting from cell proliferation in tissue repair.