PMID- 20818496
OWN - NLM
STAT- MEDLINE
DCOM- 20110110
LR  - 20190606
IS  - 1791-244X (Electronic)
IS  - 1107-3756 (Linking)
VI  - 26
IP  - 4
DP  - 2010 Oct
TI  - Osteoclast activation by receptor activator of NF-kappaB ligand enhances the 
      mobilization of hematopoietic progenitor cells from the bone marrow in acute 
      injury.
PG  - 557-63
AB  - Osteoclasts (OCLs) are multinucleated cells that are derived from the 
      monocyte/macrophage hematopoietic lineage in response to receptor activator of 
      NF-kappaB ligand (RANKL) activation. They are specialized cells responsible for 
      physiological bone resorption and as well as pathologic bone loss. In addition to 
      their unique ability to resorb bone, OCLs also play a potential role in the 
      mobilization of hematopoietic progenitor cells from the bone marrow (BM), 
      particularly under various stress stimuli (e.g. hypoxia, injury or inflammation). 
      We investigated the effect of activated OCLs on the stem cell niche and whether 
      this leads to mobilization of hematopoietic progenitors. We induced activated 
      OCLs from the RAW264.7 cell line through stimulation with RANKL and we quantified 
      the levels of the stem cell niche component SDF-1 on the osteblasts and CXCR4 on 
      the bone marrow cells (BMCs) by culturing with supernatants from activated OCLs. 
      In addition, we exposed mice to stress by inducing liver injury with CCl4 
      followed by injecting RANKL to activate OCLs and compared the effect on the 
      mobilization of hematopoietic progenitor cells from the BM. We found that 
      functional OCLs cleaved SDF-1alpha in the osteoblasts and increased CXCR4 
      expression in the BMCs. Moreover, under stress in vivo, mobilized hematopoietic 
      progenitor cells were significantly increased after RANKL treatment. These 
      results suggest that OCLs might be involved in alteration of the interaction 
      between SDF-1 and CXCR4 leading to mobilization of hematopoietic progenitor cells 
      from the BM.
FAU - Cho, Kyung-Ah
AU  - Cho KA
AD  - Department of Microbiology, School of Medicine, Ewha Womans University, Seoul, 
      Korea.
FAU - Joo, Sun-Young
AU  - Joo SY
FAU - Han, Ho-Seong
AU  - Han HS
FAU - Ryu, Kyung-Ha
AU  - Ryu KH
FAU - Woo, So-Youn
AU  - Woo SY
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Greece
TA  - Int J Mol Med
JT  - International journal of molecular medicine
JID - 9810955
RN  - 0 (Chemokine CXCL12)
RN  - 0 (Receptor Activator of Nuclear Factor-kappa B)
RN  - 0 (Receptors, CXCR4)
SB  - IM
MH  - Animals
MH  - Cell Differentiation
MH  - Cell Line
MH  - Chemokine CXCL12/*metabolism
MH  - Female
MH  - Hematopoietic Stem Cells/*cytology/metabolism
MH  - Liver/*injuries
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Osteoclasts/*cytology/metabolism
MH  - Receptor Activator of Nuclear Factor-kappa B/*metabolism
MH  - Receptors, CXCR4/*metabolism
EDAT- 2010/09/08 06:00
MHDA- 2011/01/11 06:00
CRDT- 2010/09/07 06:00
PHST- 2010/09/07 06:00 [entrez]
PHST- 2010/09/08 06:00 [pubmed]
PHST- 2011/01/11 06:00 [medline]
AID - 10.3892/ijmm_00000499 [doi]
PST - ppublish
SO  - Int J Mol Med. 2010 Oct;26(4):557-63. doi: 10.3892/ijmm_00000499.