Expression and functional role of formyl peptide receptor in human bone marrow-derived mesenchymal stem cells

Mi Kyoung Kim; Do Sik Min; Yoon Jeong Park; Jae Ho Kim; Sung Ho Ryu; Yoe Sik Bae

doi:10.1016/j.febslet.2007.03.078

Expression and functional role of formyl peptide receptor in human bone marrow-derived mesenchymal stem cells

Mi Kyoung Kim, Do Sik Min, Yoon Jeong Park, Jae Ho Kim, Sung Ho Ryu, Yoe Sik Bae

Department of Pharmacy

Research output: Contribution to journal › Article

19 Citations (Scopus)

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.

Original language	English
Pages (from-to)	1917-1922
Number of pages	6
Journal	FEBS Letters
Volume	581
Issue number	9
DOIs	https://doi.org/10.1016/j.febslet.2007.03.078
Publication status	Published - 2007 May 1

Fingerprint

All Science Journal Classification (ASJC) codes

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

Cite this

Kim, M. K., Min, D. S., Park, Y. J., Kim, J. H., Ryu, S. H., & Bae, Y. S. (2007). Expression and functional role of formyl peptide receptor in human bone marrow-derived mesenchymal stem cells. FEBS Letters, 581(9), 1917-1922. https://doi.org/10.1016/j.febslet.2007.03.078

@article{9349996858194c00a6333c6909464cfc,

title = "Expression and functional role of formyl peptide receptor in human bone marrow-derived mesenchymal stem cells",

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.",

author = "Kim, {Mi Kyoung} and Min, {Do Sik} and Park, {Yoon Jeong} and Kim, {Jae Ho} and Ryu, {Sung Ho} and Bae, {Yoe Sik}",

year = "2007",

month = may

day = "1",

doi = "10.1016/j.febslet.2007.03.078",

language = "English",

volume = "581",

pages = "1917--1922",

journal = "FEBS Letters",

issn = "0014-5793",

publisher = "Elsevier",

number = "9",

}

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 -

Access to Document

10.1016/j.febslet.2007.03.078