{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T20:39:04Z","timestamp":1791405544858,"version":"4.3.3"},"reference-count":57,"publisher":"BMJ","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Gut"],"accepted":{"date-parts":[[2010,10,18]]},"published-print":{"date-parts":[[2011,4]]},"abstract":"<jats:sec>\n                    <jats:title>Background and methods<\/jats:title>\n                    <jats:p>\n                      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 I\u03b11\n                      <jats:sup>(r\/r)<\/jats:sup>\n                      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.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Chronic fibrotic carbon tetrachloride (CCl\n                      <jats:sub>4<\/jats:sub>\n                      ) injury can induce a florid HPC response associated with dense laminin deposition. In the recovery phase after chronic CCl\n                      <jats:sub>4<\/jats:sub>\n                      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.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/gut.2010.224436","type":"journal-article","created":{"date-parts":[[2010,11,24]],"date-time":"2010-11-24T20:26:57Z","timestamp":1290630417000},"page":"525-533","source":"Crossref","is-referenced-by-count":93,"title":["Remodelling of extracellular matrix is a requirement for the hepatic progenitor cell response"],"prefix":"10.1136","volume":"60","author":[{"given":"Yiannis N","family":"Kallis","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew J","family":"Robson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jonathan A","family":"Fallowfield","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Howard 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