Back to Search
Start Over
SDF-1 increases recruitment of osteoclast precursors by upregulation of matrix metalloproteinase-9 activity.
- Source :
-
Connective tissue research [Connect Tissue Res] 2003; Vol. 44 Suppl 1, pp. 79-84. - Publication Year :
- 2003
-
Abstract
- Although chemokines play essential roles in the trafficking and homing of many circulating hematopoietic cell types, their potential influences on osteoclast (OC) recruitment or bone remodeling are not well known. Therefore, chemokine receptor expression was analyzed by RNase protection assay during OC formation induced by RANKL in a murine mononuclear cell line (RAW 264.7). Relatively high CXCR4 expression was detected in RAW cells (pre-OCs), whereas CXCR4 levels were downregulated during RAW-OC development. SDF-1, the unique ligand for CXCR4, stimulated RAW cell production of matrix metalloproteinase (MMP)-9 activity, a matrix-degrading enzyme essential for pre-OC migration into the developing bone marrow cavity. Induced MMP-9 activity in RAW cells was associated with their increased MMP-dependent transmigration through a collagen gel in response to SDF-1. We conclude that SDF-1 stimulation of MMP-9 activity in pre-OCs may be a key aspect of their recruitment to bone and migration within the marrow to sites for OC differentiation and bone resorption.
- Subjects :
- Animals
Carrier Proteins pharmacology
Cell Differentiation drug effects
Cell Line
Chemokine CXCL12
Macrophages
Membrane Glycoproteins pharmacology
Mice
Osteoclasts cytology
Osteoclasts enzymology
RANK Ligand
RNA, Messenger metabolism
Receptor Activator of Nuclear Factor-kappa B
Receptors, CXCR4 biosynthesis
Receptors, CXCR4 genetics
Stem Cells cytology
Stem Cells enzymology
Up-Regulation
Cell Movement drug effects
Chemokines, CXC pharmacology
Matrix Metalloproteinase 9 biosynthesis
Osteoclasts drug effects
Stem Cells drug effects
Subjects
Details
- Language :
- English
- ISSN :
- 0300-8207
- Volume :
- 44 Suppl 1
- Database :
- MEDLINE
- Journal :
- Connective tissue research
- Publication Type :
- Academic Journal
- Accession number :
- 12952178