{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,11]],"date-time":"2026-05-11T12:32:00Z","timestamp":1778502720044,"version":"3.51.4"},"reference-count":39,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2014,6,26]],"date-time":"2014-06-26T00:00:00Z","timestamp":1403740800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001659","name":"German Research Foundation","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Liver International"],"published-print":{"date-parts":[[2015,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background &amp; Aims<\/jats:title><jats:p>Matrilins are a family of four oligomeric adaptor proteins whose functions in extracellular matrix assembly during pathophysiological events still need to be explored in more detail. Matrilin\u20102 is the largest family member and the only matrilin expressed in the naive liver. Several studies demonstrate that matrilin\u20102 interacts with collagen I, fibronectin or laminin\u2010111\u2010nidogen\u20101 complexes. All these matrix components get upregulated during hepatic scar tissue formation. Therefore, we tested whether matrilin\u20102 has an influence on the formation and\/or the resolution of fibrotic tissue in the mouse liver.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Fibrosis was induced by infection with an adenovirus encoding cytochrome P450 2D6 (autoimmune liver damage) or by exposure to the hepatotoxin carbon tetrachloride. Fibrosis severity and matrilin\u20102 expression were assessed by immunohistochemistry. Hepatic stellate cells (<jats:styled-content style=\"fixed-case\">HSC<\/jats:styled-content>s) were isolated and analysed by immunocytochemistry and Transwell migration assays.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Both autoimmune as well as chemically induced liver damage led to simultaneous upregulation of matrilin\u20102 and collagen I expression. Discontinuation of carbon tetrachloride exposure resulted in concomitant dissolution of both proteins. Activated <jats:styled-content style=\"fixed-case\">HSC<\/jats:styled-content>s were the source of <jats:italic>de novo<\/jats:italic> matrilin\u20102 expression. Comparing wild type and matrilin\u20102\u2010deficient mice, no differences were detected in fibronectin and collagen I upregulation and resolution kinetics as well as amount or location of fibronectin and collagen I production and degradation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Our findings suggest that the absence of matrilin\u20102 has no effect on <jats:styled-content style=\"fixed-case\">HSC<\/jats:styled-content> activation and regression kinetics, synthetic activity, proliferative capacity, motility, or <jats:styled-content style=\"fixed-case\">HSC<\/jats:styled-content> apoptosis.<\/jats:p><\/jats:sec>","DOI":"10.1111\/liv.12604","type":"journal-article","created":{"date-parts":[[2014,6,6]],"date-time":"2014-06-06T10:36:47Z","timestamp":1402051007000},"page":"1265-1273","source":"Crossref","is-referenced-by-count":5,"title":["Upregulation of matrilin\u20102 expression in murine hepatic stellate cells during liver injury has no effect on 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