title: [Exenatide promotes chemotactic migration of adipose-derived stem cells through SDF-1/CXCR-4/Rho GTPase pathway].
abstract: OBJECTIVE
  To investigate the effect of exenatide on chemotactic migration of adipose-derived stem cells (ADSCs) and confirm that Rho GTPase is the downstream effector protein of SDF-1/CXCR-4 migration pathway.
  
  
  METHODS
  ADSCs were isolated, cultured, identified by flow cytometry, and induced to differentiate in vitro. RTCA xCELLigence system was used to analyze the effect of exenatide on ADSC proliferation. The effects of exenatide at different concentrations, AMD3100 (CXCR-4 antagonist), and CCG-1423 (Rho GTPase antagonist) on chemotactic migration of ADSCs were tested using Transwell assay. The expression of CXCR-4 in exenatide-treated ADSCs was measured by flow cytometry and Western blotting. Active Rho pull-down detection kit was used to detect the expression of Rho GTPase. Laser confocal microscopy was used to observe the formation of stress fibers in ADSCs with different treatments.
  
  
  RESULTS
  Exenatide treatment for 24 h had no significant effect on ADSC proliferation. Exenatide obviously promoted chemotactic migration of ADSCs in a concentration-dependent manner, and this effect was blocked by either AMD3100 or CCG-1423. Both flow cytometry and Western blotting showed that exenatide dose-dependently up-regulated CXCR-4 expression in ADSCs. Western blotting showed that the expression of Rho GTPase was related to SDF-1/CXCR-4 pathway, and laser confocal microscopy revealed that the formation of stress fibers in ADSCs was related to SDF-1/CXCR-4/ Rho GTPase pathway.
  
  
  CONCLUSIONS
  Exenatide promotes chemotactic migration of ADSCs, and Rho GTPase is the downstream effector protein of SDF-1/CXCR-4 pathway.
authors: Department of Cardiology, General Hospital of PLA, Beijing 100853, China. E-mail: robustma@163.com.
authors: Qiang
authors: Q
authors: Ma
authors: Jun-Jie
authors: JJ
authors: Yang
authors: Hao
authors: H
authors: Zhou
authors: Ying
authors: Y
authors: Zhang
authors: Yun-Dai
authors: YD
authors: Chen
mesh_terms: D000273:Adipose Tissue / Q000166:cytology*; D000813:Anilides / Q000494:pharmacology; D001549:Benzamides / Q000494:pharmacology; D001596:Benzylamines; D002478:Cells, Cultured; D054377:Chemokine CXCL12 / Q000378:metabolism*; D002633:Chemotaxis; D000080027:Cyclams; D000077270:Exenatide; D006571:Heterocyclic Compounds / Q000494:pharmacology; D006801:Humans; D010455:Peptides / Q000494:pharmacology*; D019718:Receptors, CXCR4 / Q000037:antagonists & inhibitors / Q000378:metabolism*; D015398:Signal Transduction; D013234:Stem Cells / Q000166:cytology*; D014688:Venoms / Q000494:pharmacology*; D020741:rho GTP-Binding Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism*
chemical_list: D000813:Anilides; D001549:Benzamides; D001596:Benzylamines; C523455:CCG 1423; C515255:CXCL12 protein, human; C527276:CXCR4 protein, human; D054377:Chemokine CXCL12; D000080027:Cyclams; D006571:Heterocyclic Compounds; D010455:Peptides; D019718:Receptors, CXCR4; D014688:Venoms; D000077270:Exenatide; D020741:rho GTP-Binding Proteins; C088327:plerixafor