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Title: Insulin-like growth factor 1 enhances the migratory capacity of mesenchymal stem cells

Journal Article · · Biochemical and Biophysical Research Communications
 [1];  [2];  [2];  [2];  [3];  [4]
  1. Laboratory of Heart Failure and Stem Cell, Texas Heart Institute, Houston, TX 77030 (United States)
  2. Research Center of Medical Sciences, Guangdong Provincial People's Hospital, Guangdong Provincial Cardiovascular Institute, Guanzhou, Guandong 510080 (China)
  3. Section of Cardiology, Xiangya Hospital of Central-South University, Changsha, Hunan 410008 (China)
  4. Department of Molecular Pathology, University of Texas M.D. Anderson Cancer Center, Houston, TX 77030 (United States)

Mesenchymal stem cells (MSCs) are attractive candidates for cell based therapies. However, the mechanisms responsible for stem cell migration and homing after transplantation remain unknown. It has been shown that insulin-like growth factor-1 (IGF-1) induces proliferation and migration of some cell types, but its effects on stem cells have not been investigated. We isolated and cultured MSC from rat bone marrow, and found that IGF-1 increased the expression levels of the chemokine receptor CXCR4 (receptor for stromal cell-derived factor-1, SDF-1). Moreover, IGF-1 markedly increased the migratory response of MSC to SDF-1. The IGF-1-induced increase in MSC migration in response to SDF-1 was attenuated by PI3 kinase inhibitor (LY294002 and wortmannin) but not by mitogen-activated protein/ERK kinase inhibitor PD98059. Our data indicate that IGF-1 increases MSC migratory responses via CXCR4 chemokine receptor signaling which is PI3/Akt dependent. These findings provide a new paradigm for biological effects of IGF-1 on MSC and have implications for the development of novel stem cell therapeutic strategies.

OSTI ID:
20991338
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 356, Issue 3; Other Information: DOI: 10.1016/j.bbrc.2007.03.049; PII: S0006-291X(07)00523-2; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English