2007
DOI: 10.1002/hep.21477
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Bone marrow–derived cells express matrix metalloproteinases and contribute to regression of liver fibrosis in mice

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Cited by 240 publications
(215 citation statements)
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“…Infusion of bone marrow‐derived macrophages has been shown to reduce hepatic fibrosis by recruiting endogenous macrophages and neutrophils 3. Administration of granulocyte colony‐stimulating factor enhanced migration of bone marrow cells into fibrotic liver and accelerated the regression of liver fibrosis 24. It was also reported that depletion of neutrophils by polymorphonuclear cell‐specific antibody treatment blocked degradation of collagen during the recovery process of reversible biliary obstruction in rats 25.…”
Section: Discussionmentioning
confidence: 99%
“…Infusion of bone marrow‐derived macrophages has been shown to reduce hepatic fibrosis by recruiting endogenous macrophages and neutrophils 3. Administration of granulocyte colony‐stimulating factor enhanced migration of bone marrow cells into fibrotic liver and accelerated the regression of liver fibrosis 24. It was also reported that depletion of neutrophils by polymorphonuclear cell‐specific antibody treatment blocked degradation of collagen during the recovery process of reversible biliary obstruction in rats 25.…”
Section: Discussionmentioning
confidence: 99%
“…35 Although it is beyond the scope of this article to determine whether the CCR2-positive cells that participate in the resolution of fibrosis come from the bone marrow, the fact that monocyte emigration from bone marrow requires signals mediated by chemokine receptor CCR2 argues for this hypothesis. [15][16][17] The mirrored distribution pattern of F4/80 ϩ CD11b ϩ that we observed in blood and in bone marrow (ie, CCR2 Ϫ/Ϫ mice have higher proportions in bone marrow but lower in blood) supports this assumption.…”
Section: Discussionmentioning
confidence: 99%
“…They can therefore address (1) HSC activation and recruitment, (2) activation of cells upstream of HSC activation, (3) profibrogenic growth factors, cytokines and other mediators, (4) intracellular profibrogenic pathways in HSC and cells upstream of their activation, and (5) stimulation of fibrolytic processes to reverse existing fibrosis. Recently it has become evident that activated HSC (myofibroblasts) can also originate from periportal or perivascular fibroblasts, 5,6 bone marrow-derived circulating fibrocytes 7,8 that are recruited from the bloodstream during chronic liver injury, or from liver epithelia by way of the process of epithelial-to-mesenchymal transition (EMT) 9,10 ( Fig. 1).…”
Section: Promising Targets For Antifibrotic Therapiesmentioning
confidence: 99%