NDLI: Hepatocyte growth factor/c-met signaling pathway is required for efficient liver regeneration and repair.

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Hepatocyte growth factor/c-met signaling pathway is required for efficient liver regeneration and repair.

Content Provider	Semantic Scholar
Author	Factor, Valentina M. Sánchez, Aránzazu Pérez Uchida, Koichi Conner, Elizabeth A. Thorgeirsson, Snorri
Copyright Year	2004
Abstract	Hepatocyte growth factor/scatter factor c-met signaling pathway is of central importance during development as well as in tumorigenesis. Because homozygous null mice for either hgf/sf or c-met die in utero, we used Cre/loxP-mediated gene targeting to investigate the function of c-met specifically in the adult liver. Loss of c-met appeared not to be detrimental to hepatocyte function under physiological conditions. Nonetheless, the adaptive responses of the liver to injury were dramatically affected. Mice lacking c-met gene in hepatocytes were hypersensitive to Fas-induced apoptosis. When injected with a low dose of anti-Fas antibody, the majority of these mice died from massive apoptosis and hemorrhagic necrosis, whereas all wild-type mice survived with signs of minor injury. After a challenge with a single necrogenic dose of CCl4, c-met conditional knockout mice exhibited impaired recovery from centrolobular lesions rather than a deficit in hepatocyte proliferation. The delayed healing was associated with a persistent inflammatory reaction, over-production of osteopontin, early and prominent dystrophic calcification, and impaired hepatocyte scattering/migration into diseased areas. These studies provide direct genetic evidence in support of the critical role of c-met in efficient liver regeneration and suggest that disruption of c-met affects primarily hepatocyte survival and tissue remodeling.
File Format	PDF HTM / HTML
DOI	10.1073/pnas.0306068101
PubMed reference number	15070743
Journal	Medline
Volume Number	101
Issue Number	13
Alternate Webpage(s)	http://www.pnas.org/content/101/13/4477.full.pdf
Alternate Webpage(s)	https://doi.org/10.1073/pnas.0306068101
Journal	Proceedings of the National Academy of Sciences of the United States of America
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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