| Literature DB >> 17442310 |
Mi-Kyoung Kim1, Do Sik Min, Yoon Jeong Park, Jae Ho Kim, Sung Ho Ryu, Yoe-Sik Bae.
Abstract
We investigated the expression of formyl peptide receptor (FPR) and its functional role in human bone marrow-derived mesenchymal stem cells (MSCs). We analyzed the expression of FPR by using ligand-binding assay with radio-labeled N-formyl-met-leu-phe (fMLF), and found that MSCs express FPR. FMLF stimulated intracellular calcium increase, mitogen-activated protein kinases activation, and Akt activation, which were mediated by G(i) proteins. MSCs were chemotactically migrated to fMLF. FMLF-induced MSC chemotaxis was also completely inhibited by pertussis toxin, LY294002, and PD98059, indicating the role of G(i) proteins, phosphoinositide 3-kinase, and extracellular signal regulated protein kinase. N-terminal fragment of annexin-1, Anx-1(2-26), an endogenous agonist for FPR, also induced chemotactic migration of MSCs. Thus MSCs express functional FPR, suggesting a new (patho)physiological role of FPR and its ligands in regulating MSC trafficking during induction of injured tissue repair.Entities:
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Year: 2007 PMID： 17442310 DOI： 10.1016/j.febslet.2007.03.078
Source DB: PubMed Journal: FEBS Lett ISSN： 0014-5793 Impact factor: 4.124