2009
DOI: 10.1172/jci36541
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MT1-MMP and RECK are involved in human CD34+ progenitor cell retention, egress, and mobilization

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Cited by 95 publications
(102 citation statements)
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References 53 publications
(50 reference statements)
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“…In this regard, G-CSF signaling induces PI3K-mediated Akt phosphorylation, increasing membrane type 1-matrix metalloproteinase (MT1-MMP) expression. MT1-MMP-mediated CD44 proteolysis then results in human CD34+ progenitor cell egression and mobilization (Vagima et al, 2009). Further investigation will be necessary to understand the precise mechanism underlying the priming effect of TNF-α pretreatment on the migratory capability of hAdMSCs.…”
Section: Discussionmentioning
confidence: 99%
“…In this regard, G-CSF signaling induces PI3K-mediated Akt phosphorylation, increasing membrane type 1-matrix metalloproteinase (MT1-MMP) expression. MT1-MMP-mediated CD44 proteolysis then results in human CD34+ progenitor cell egression and mobilization (Vagima et al, 2009). Further investigation will be necessary to understand the precise mechanism underlying the priming effect of TNF-α pretreatment on the migratory capability of hAdMSCs.…”
Section: Discussionmentioning
confidence: 99%
“…A number of active proteases, including neutrophil elastase, cathepsin G, matrix metalloproteinase (MMP)-9, MMP14, and plasmin, are increased in the bone marrow following G-CSF or chemotherapy administration, largely secondary to the dramatic increase in maturing myeloid cells [43][44][45]. Furthermore, endogenous protease inhibitors, such as serpin A1 and serpin A3, are significantly reduced in the bone marrow following G-CSF administration [46] resulting in a highly proteolytic environment.…”
Section: Proteasesmentioning
confidence: 99%
“…In addition to cleaving and inactivating CXCL12 [36], bone marrow proteases also cleave other molecules thought to be involved in HSC retention in the bone marrow. Perhaps, the most prominent of these are adhesion molecules important for the retention of HSC, including CD44 and VCAM-1, and the cytokine receptor c-kit (Table 1) [45,47,48].…”
Section: Proteasesmentioning
confidence: 99%
“…Oxidized low-density lipoprotein decreased the survival of EPCs and impaired their function through decreased endothelial nitric oxide synthetase expression 15) . EPC mobilization occurs also through matrix metalloproteinase-mediated mechanisms [16][17][18] . Matrix metalloproteinase species activate local protease activity and weaken stromal cell-EPC interactions in the bone marrow.…”
Section: Introductionmentioning
confidence: 99%
“…Matrix metalloproteinase species activate local protease activity and weaken stromal cell-EPC interactions in the bone marrow. Membrane type-1 matrix metalloproteinase (MT1-MMP), which contributes to vascular remodeling and atherosclerotic plaque disruption 19) , was shown to regulate the mobilization of CD34 progenitor cells from the bone marrow in a mouse model 17) . In spite of the occurrence of endothelial dysfunction in peripheral artery disease (PAD), little information is available on EPC mobilization in these patients according to clinical status.…”
Section: Introductionmentioning
confidence: 99%