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 |
Fingerprint
All Science Journal Classification (ASJC) codes
- Biophysics
- Structural Biology
- Biochemistry
- Molecular Biology
- Genetics
- Cell Biology
Cite this
}
Expression and functional role of formyl peptide receptor in human bone marrow-derived mesenchymal stem cells. / Kim, Mi Kyoung; Min, Do Sik; Park, Yoon Jeong; Kim, Jae Ho; Ryu, Sung Ho; Bae, Yoe Sik.
In: FEBS Letters, Vol. 581, No. 9, 01.05.2007, p. 1917-1922.Research output: Contribution to journal › Article
TY - JOUR
T1 - Expression and functional role of formyl peptide receptor in human bone marrow-derived mesenchymal stem cells
AU - Kim, Mi Kyoung
AU - Min, Do Sik
AU - Park, Yoon Jeong
AU - Kim, Jae Ho
AU - Ryu, Sung Ho
AU - Bae, Yoe Sik
PY - 2007/5/1
Y1 - 2007/5/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=34247141961&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=34247141961&partnerID=8YFLogxK
U2 - 10.1016/j.febslet.2007.03.078
DO - 10.1016/j.febslet.2007.03.078
M3 - Article
C2 - 17442310
AN - SCOPUS:34247141961
VL - 581
SP - 1917
EP - 1922
JO - FEBS Letters
JF - FEBS Letters
SN - 0014-5793
IS - 9
ER -