Literature DB >> 21106552

Remodelling of extracellular matrix is a requirement for the hepatic progenitor cell response.

Yiannis N Kallis1, Andrew J Robson, Jonathan A Fallowfield, Howard C Thomas, Malcolm R Alison, Nicholas A Wright, Robert D Goldin, John P Iredale, Stuart J Forbes.   

Abstract

BACKGROUND AND METHODS: In advanced liver damage, hepatic regeneration can occur through proliferation of a resident hepatic progenitor cell (HPC) population. HPCs are located within a designated niche in close association with myofibroblasts and bone marrow (BM) derived macrophages. Extra-cellular matrix (ECM) laminin invariably surrounds HPCs, but the functional requirement of this matrix-cell association is untested in vivo. Using the collagen Iα1((r/r)) mouse (r/r), which produces mutated collagen I resistant to matrix metalloproteinase degradation and has an exaggerated fibrotic response to liver injury, we test the relationship between collagen degradation, laminin deposition, and the HPC response.
RESULTS: Chronic fibrotic carbon tetrachloride (CCl₄) injury can induce a florid HPC response associated with dense laminin deposition. In the recovery phase after chronic CCl₄ injury, r/r mice have a markedly attenuated HPC response compared to wild-types, together with persistence of collagen I and failure to deposit ECM laminin. Similar results were found in r/r mice given the choline-deficient ethionine supplemented diet, another model of the HPC response. In cross-over sex-mismatched BM transplantation (BMT) experiments between r/r mice and wild-types, the blunted HPC response of r/r mice was not rescued by wild-type BMT and likewise not conferred on to wild-type recipients by r/r BMT, demonstrating that the attenuated HPC response in r/r mice is a property intrinsic to the liver.
CONCLUSION: Failure of ECM remodelling after chronic fibrotic liver injury hinders the ability of the liver to activate HPCs. Laminin-progenitor cell interactions within the HPC niche are a critical for HPC mediated regeneration.

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Year:  2010        PMID: 21106552     DOI: 10.1136/gut.2010.224436

Source DB:  PubMed          Journal:  Gut        ISSN: 0017-5749            Impact factor:   23.059


  47 in total

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