Hintermann, Edith, Bayer, Monika, Pfeilschifter, Josef M., Deak, Ferenc, Kiss, Ibolya, Paulsson, Mats and Christen, Urs ORCID: 0000-0003-4165-7976 (2015). Upregulation of matrilin-2 expression in murine hepatic stellate cells during liver injury has no effect on fibrosis formation and resolution. Liver Int., 35 (4). S. 1265 - 1274. HOBOKEN: WILEY. ISSN 1478-3231

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Abstract

Background & AimsMatrilins 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-2 is the largest family member and the only matrilin expressed in the naive liver. Several studies demonstrate that matrilin-2 interacts with collagen I, fibronectin or laminin-111-nidogen-1 complexes. All these matrix components get upregulated during hepatic scar tissue formation. Therefore, we tested whether matrilin-2 has an influence on the formation and/or the resolution of fibrotic tissue in the mouse liver. MethodsFibrosis 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-2 expression were assessed by immunohistochemistry. Hepatic stellate cells (HSCs) were isolated and analysed by immunocytochemistry and Transwell migration assays. ResultsBoth autoimmune as well as chemically induced liver damage led to simultaneous upregulation of matrilin-2 and collagen I expression. Discontinuation of carbon tetrachloride exposure resulted in concomitant dissolution of both proteins. Activated HSCs were the source of de novo matrilin-2 expression. Comparing wild type and matrilin-2-deficient 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. ConclusionsOur findings suggest that the absence of matrilin-2 has no effect on HSC activation and regression kinetics, synthetic activity, proliferative capacity, motility, or HSC apoptosis.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Hintermann, EdithUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Bayer, MonikaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Pfeilschifter, Josef M.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Deak, FerencUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Kiss, IbolyaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Paulsson, MatsUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Christen, UrsUNSPECIFIEDorcid.org/0000-0003-4165-7976UNSPECIFIED
URN: urn:nbn:de:hbz:38-404306
DOI: 10.1111/liv.12604
Journal or Publication Title: Liver Int.
Volume: 35
Number: 4
Page Range: S. 1265 - 1274
Date: 2015
Publisher: WILEY
Place of Publication: HOBOKEN
ISSN: 1478-3231
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
AUTOANTIGEN CYTOCHROME-P450 2D6; MATRIX PROTEIN; HEPATOCELLULAR-CARCINOMA; TISSUE DISTRIBUTION; MOLECULAR-STRUCTURE; MICE LACKING; MOUSE MODEL; REGENERATION; FIBROGENESIS; TOLERANCEMultiple languages
Gastroenterology & HepatologyMultiple languages
URI: http://kups.ub.uni-koeln.de/id/eprint/40430

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