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 › peer-review

23 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

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

Access to Document

10.1016/j.febslet.2007.03.078

Fingerprint Dive into the research topics of 'Expression and functional role of formyl peptide receptor in human bone marrow-derived mesenchymal stem cells'. Together they form a unique fingerprint.

Cite this

@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}",

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.",

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

N1 - 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.

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 -

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

Abstract

Bibliographical note

All Science Journal Classification (ASJC) codes

Access to Document

Other files and links

Cite this