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 Gi 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 Gi 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.
| Original language | English |
|---|---|
| Pages (from-to) | 1917-1922 |
| Number of pages | 6 |
| Journal | FEBS Letters |
| Volume | 581 |
| Issue number | 9 |
| DOIs | |
| Publication status | Published - 2007 May 1 |
Bibliographical note
Funding Information:This work was supported by a grant 02-PJ2-PG1-CH16-0002 from the Korea Health 21 R&D Project, Ministry of Health & Welfare, Republic of Korea, the Korea Science and Engineering Foundation through the Medical Science and Engineering Research Center for Cancer Molecular Therapy at Dong-A University, and by a grant of Biotechnology Development Program (Grant Number 2005-00115) from Ministry of Science and Technology (MOST), Republic of Korea.
All Science Journal Classification (ASJC) codes
- Biophysics
- Structural Biology
- Biochemistry
- Molecular Biology
- Genetics
- Cell Biology