PMID- 21678414
OWN - NLM
STAT- MEDLINE
DCOM- 20120305
LR  - 20161125
IS  - 1097-4652 (Electronic)
IS  - 0021-9541 (Linking)
VI  - 227
IP  - 4
DP  - 2012 Apr
TI  - Absence of MCP-1 leads to elevated bone mass via impaired actin ring formation.
PG  - 1619-27
LID - 10.1002/jcp.22879 [doi]
AB  - Monocyte chemoattractant protein-1 (MCP-1) is associated with various 
      inflammatory diseases involving bone loss, and is expressed along with its 
      receptor by bone marrow-derived macrophages (BMM), which are osteoclast (OC) 
      precursors. To investigate the role of MCP-1 in bone remodeling, we compared 
      MCP-1-knockout (KO) mice with wild-type (WT) mice. The absence of MCP-1 increased 
      bone mass and lowered serum collagen type I fragments (CTX-1) and TRACP 5b, but 
      had no significant effect on the N-terminal propeptide of type I procollagen, 
      suggesting that OCs are primarily responsible for the bone phenotype observed in 
      the absence of MCP-1. MCP-1 deficiency resulted in reduced numbers and activity 
      of OCs in vitro. It also led to a reduced level of c-Fms and receptor activator 
      of nuclear factor-kappaB receptor and impaired actin ring formation. Activation of 
      ERK, Akt, Rac1, and Rho upon M-CSF stimulation was also reduced and our evidence 
      suggests that the aberrant actin ring formation was partly due to reduced 
      activation of these molecules. Our findings point to a role of osteoclast MCP-1 
      in regulating bone remodeling. The higher bone mass in the femurs of MCP-1-KO 
      mice could be, at least in part, due to decreased osteoclastogenesis and bone 
      resorption resulting from aberrant M-CSF signaling in OCs.
CI  - Copyright (c) 2011 Wiley Periodicals, Inc.
FAU - Sul, Ok-Joo
AU  - Sul OJ
AD  - Department of Biological Sciences (BK21 Program) and the Immunomodulation 
      Research Center, University of Ulsan, Ulsan, Korea.
FAU - Ke, Ke
AU  - Ke K
FAU - Kim, Woon-Ki
AU  - Kim WK
FAU - Kim, Song-Hee
AU  - Kim SH
FAU - Lee, Sang-Chul
AU  - Lee SC
FAU - Kim, Hyun-Ju
AU  - Kim HJ
FAU - Kim, Shin-Yoon
AU  - Kim SY
FAU - Suh, Jae-Hee
AU  - Suh JH
FAU - Choi, Hye-Seon
AU  - Choi HS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Actins)
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (DNA Primers)
RN  - 81627-83-0 (Macrophage Colony-Stimulating Factor)
SB  - IM
MH  - Actins/*metabolism
MH  - Animals
MH  - Base Sequence
MH  - Bone Remodeling/genetics/*physiology
MH  - Bone Resorption/metabolism/pathology
MH  - Bone and Bones/anatomy & histology/diagnostic imaging
MH  - Chemokine CCL2/*deficiency/genetics/metabolism
MH  - DNA Primers/genetics
MH  - Female
MH  - Macrophage Colony-Stimulating Factor/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Osteoclasts/cytology/metabolism
MH  - Signal Transduction
MH  - Stem Cells/cytology/metabolism
MH  - X-Ray Microtomography
EDAT- 2011/06/17 06:00
MHDA- 2012/03/06 06:00
CRDT- 2011/06/17 06:00
PHST- 2011/06/17 06:00 [entrez]
PHST- 2011/06/17 06:00 [pubmed]
PHST- 2012/03/06 06:00 [medline]
AID - 10.1002/jcp.22879 [doi]
PST - ppublish
SO  - J Cell Physiol. 2012 Apr;227(4):1619-27. doi: 10.1002/jcp.22879.