Type XVIII collagen is essential for survival during acute liver injury in mice
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Duncan-2013-Type XVIII collagen.pdf
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Author(s)
Duncan, Michael B.
Yang, Changqing
Tanjore, Harikrishna
Boyle, Patrick M.
Keskin, Doruk
Sugimoto, Hikaru
Zeisberg, Michael
Olsen, Bjorn R.
Kalluri, Raghu
Date Issued
April 2013
Journal
Disease Models & Mechanisms
Publisher
Company of Biologists, Ltd.
Citation
Duncan, M. B., C. Yang, H. Tanjore, P. M. Boyle, D. Keskin, H. Sugimoto, M. Zeisberg, B. R. Olsen, and R. Kalluri. “Type XVIII Collagen Is Essential for Survival During Acute Liver Injury in Mice.” Disease Models & Mechanisms 6, no. 4 (April 4, 2013): 942–951.
Version
Final published version
Abstract
The regenerative response to drug- and toxin-induced liver injury induces changes to the hepatic stroma, including the extracellular matrix. Although the extracellular matrix is known to undergo changes during the injury response, its impact on maintaining hepatocyte function and viability in this process remains largely unknown. We demonstrate that recovery from toxin-mediated injury is impaired in mice deficient in a key liver extracellular matrix molecule, type XVIII collagen, and results in rapid death. The type-XVIII-collagen-dependent response to liver injury is mediated by survival signals induced by α1β1 integrin, integrin linked kinase and the Akt pathway, and mice deficient in either α1β1 integrin or hepatocyte integrin linked kinase also succumb to toxic liver injury. These findings demonstrate that type XVIII collagen is an important functional component of the liver matrix microenvironment and is crucial for hepatocyte survival during injury and stress.
MIT Department
Harvard University--MIT Division of Health Sciences and Technology
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DOI of Published Version
https://doi.org/10.1242/dmm.011577
