Effect of intercellular adhesion molecule-1 on the migration in vitro of murine mesenchymal stem cells and its related mechanism.
10.7534/j.issn.1009-2137.2014.02.039
- Author:
Yan-Guo WANG
1
,
2
;
Yue ZHAO
3
;
Xi-Mei LI
4
;
Bo TANG
4
;
Ya-Nan CHU
5
;
Yuan-Lin LIU
6
;
Heng ZHU
7
;
Yi ZHANG
8
Author Information
1. Deparment of Pathophysiology, Baotou Medical College, Baotou 014060, Inner Mongolian Autonomous Region, China
2. Institute of Basic Medical Sciences, Academy of Military Medical Sciences, Beijing 100850, China.
3. Department of Surgery, Jiuyuan Hospital of Baotou, Baotou 014060, Inner Mongolian Autonomous Region, China.
4. Training Base of Postgraduats, General Hospital of Shenyang Military Command and Liaoning Medical College, Shenyang 110016, Liaoning Province, China.
5. Department of Pediatrics, General Hospital of Tinajin Medical University,Tianjing 300052, China.
6. Institute of Basic Medical Sciences, Academy of Military Medical Sciences, Beijing 100850, Chin.
7. Institute of Basic Medical Sciences, Academy of Military Medical Sciences, Beijing 100850, Chin. E-mail: zhudingdingabc@163.com.
8. Institute of Basic Medical Sciences, Academy of Military Medical Sciences, Beijing 100850, Chin. E-mail:zhangyi612@hotmail.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Cell Line;
Cell Movement;
Intercellular Adhesion Molecule-1;
genetics;
metabolism;
MAP Kinase Signaling System;
Mesenchymal Stromal Cells;
cytology;
metabolism;
Mice;
Transfection
- From:
Journal of Experimental Hematology
2014;22(2):479-484
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to investigate the effect of intercellular adhesion molecule-1 (ICAM-1) on the migration in vitro of the murine mesenchymal stem cells (MSC) and its related mechanisms. The migration ability of murine MSC (C3H10T1/2), ICAM-1 transfected MSC (C3H10T1/2-MIGR1-ICAM-1) and empty vector-transfected MSC (C3H10T 1/2-MIGR1) were assayed in vitro by using the transwell system. Briefly, the cells were seeded on the membrane with 8 µm aperture and the fetal bovine serum was used as the chemotactic agent to induce MSC migration. The transmigrated cells were stained by crystal purple as well as DAPI for 8 h and 12 h respectively. The absolute cell numbers were counted and the migration rates of MSC were evaluated in each group. To explore the potential mechanisms which control the migration of MSC, the specific chemical inhibitors of MAPK pathway (SB203580, PD98059 and JNK inhibitor II) were added to the transwell system and the alteration of the MSC migration ability were evaluated at 12 h. The results showed that the migration ability at 8 h and 12 h of the ICAM-1-transfected MSC increased. Both absolute cell number and migration rate of MSC were significantly up-regulated by ICAM-1. Furthermore, the promoting effect of ICAM-1 on migration was partially suppressed by the inhibition of JNK/SAPK pathway. The transmigrated cell numbers and the migration rate decreased with the addition of JNK inhibitor II. However, the ICAM-1 promoting migration of MSC was not suppressed by the inhibitors for ERK/MAPK and p38/MAPK pathway did not work in the present study. It is concluded that ICAM-1 can induce mouse MSC migration in vitro, and the promoting effect is partially dependent on the activation of JNK/SAPK pathway.
