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Gastroenterology Research and Practice
Volume 2011 (2011), Article ID 727403, 8 pages
Research Article

Liver Regeneration after Partial Hepatectomy Is Not Impaired in Mice with Double Deficiency of Myd88 and IFNAR Genes

1Department of Pathology, University of Washington, Seattle, WA 98195, USA
2Laboratorio de Investigación en Hepatología y Gastroenterología, HGU Gregorio Marañón-CIBERehd, 28009 Madrid, Spain
3Department of Surgery, University of Washington, Seattle, WA 98195, USA

Received 14 July 2011; Accepted 15 September 2011

Academic Editor: Cataldo Doria

Copyright © 2011 Javier Vaquero et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Liver regeneration is known to occur in mice lacking one or more Toll-like receptors (TLRs) or the adaptor protein MyD88. Though MyD88 is required for signaling by many TLRs, others signal via MyD88-independent pathways, leading to the induction of type I interferons (IFNs). Here, we assessed liver regeneration after partial hepatectomy (PH) in mice lacking both MyD88 and the type I IFN receptor (Myd88-IFNAR double-KO). Approximately 28% of Myd88-IFNAR double-KO mice had gross liver lesions prior to surgery. In mice without lesions, Myd88-IFNAR deficiency abrogated the increase in circulating IL-6 after PH but did not impair hepatocyte BrdU incorporation, mitotic figure counts, or recovery of liver-to-body weight ratios. These results indicate that type I IFNs are not responsible for the preservation of liver regeneration in Myd88-deficient mice, and they also cast doubt on the idea of microbial products being essential triggers of liver regeneration in mice undergoing PH.