Basic Research
Copyright ©The Author(s) 2003. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Sep 15, 2003; 9(9): 2036-2039
Published online Sep 15, 2003. doi: 10.3748/wjg.v9.i9.2036
Activation of phosphorylating-p38 mitogen-activated protein kinase and its relationship with localization of intestinal stem cells in rats after ischemia-reperfusion injury
Xiao-Bing Fu, Feng Xing, Yin-Hui Yang, Tong-Zhu Sun, Bao-Chen Guo
Xiao-Bing Fu, Feng Xing, Yin-Hui Yang, Tong-Zhu Sun, Bao-Chen Guo, Wound Healing and Cell Biology Laboratory, Institute of Burns, 304 Hospital, Trauma Center of Postgraduate Medical College, Beijing 100037, China
Author contributions: All authors contributed equally to the work.
Supported by the National Basic Science and Development Program (973 Program, No. G1999054204), Grant for National Distinguished Young Scientists, No. 39525024, Grant for National Natural Science Foundation of China, No. 30170966, 30230370
Correspondence to: Xiao-Bing Fu, MD, Wound Healing and Cell Biology Laboratory, 304 Hospital, Institute of Burns, Trauma Center of Postgraduate Medical College, 51 Fu Cheng Road, Beijing 100037, China. fuxb@cgw.net.cn
Telephone: +86-10-66867396 Fax: +86-10-88416390
Received: May 10, 2003
Revised: May 23, 2003
Accepted: June 7, 2003
Published online: September 15, 2003
Abstract

AIM: To investigate the expression of phosphorylating p38 mitogen-activated protein kinase (MAPK) in rat small intestine after ischemia-reperfusion (I/R) insult and its relationship with the localization of intestinal stem cells.

METHODS: Forty-eight Wistar rats were divided randomly into three groups, namely intestinal ischemia-reperfusion group (R), intestinal ischemia group (I) and sham-operated control group (C). In group I, the animals were killed 45 minutes after superior mesenteric artery (SMA) occlusion, while in group R the rats sustained SMA occlusion for 45 minutes and reperfusion for 2, 6, 12 or 24 h respectively. In sham-operated control group, SMA was separated, but without occlusion. The activity of plasma diamine oxidase (DAO) was determined. Intestinal tissue samples were also taken for histological analysis and immunohistochemical analysis of MAPK p38 detection and intestinal stem cell localization.

RESULTS: The changes in histological structure and plasma DAO levels indicated that the intestinal barrier was damaged after intestinal I/R injury. In group C and I, each crypt contained 5-6 p38 MAPK positive cells, which were mainly located in the lower region of the crypts. This was consistent with the distribution of intestinal stem cells. The presence of positive cells in crypts increased with the time of reperfusion and reached its peak at 12 h after reperfusion (35.6%).

CONCLUSION: After intestinal I/R injury, the expression of phosphorylating-p38 MAPK in small intestine increased with the duration of reperfusion, and its distribution coincided with that of intestinal stem cells and their daughter cells, indicating that phosphorylating-p38 might be a possible marker of intestinal stem cells.

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