Journal
HEPATOLOGY
Volume 47, Issue 4, Pages 1277-1287Publisher
JOHN WILEY & SONS INC
DOI: 10.1002/hep.22129
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Funding
- NCI NIH HHS [CA53596, R01 CA053596] Funding Source: Medline
- NCRR NIH HHS [P20RR016475, P20 RR021940, P20 RR015563] Funding Source: Medline
- NIAAA NIH HHS [AA14147, R01 AA014147] Funding Source: Medline
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Pregnane X receptor (PXR) mediates xenobiotic and endobiotic metabolism as well as hepatocyte proliferation. To determine the role of PXR in liver regeneration, 2/3 partial hepatectomy (PH) was performed on wild-type and PXR-null mice. Our results showed that hepatic steatosis was markedly suppressed in mice lacking PXR 36 hours after PH, concomitant with reduction of hepatocyte proliferation at the same time point. Gene expression analysis revealed the role of PXR in regulating the transcription of genes involved in lipid uptake, transport, biosynthesis, oxidation, and storage during liver regeneration. When PXR was absent, the second wave of hepatocyte proliferation was severely suppressed, which was accompanied by the inactivation of STAT3. Lack of PXR inhibited the second phase of liver growth, leading to 17% less liver mass at the anticipated end point of liver regeneration (day 10). Conclusion: PXR is required for normal progression of liver regeneration by modulating lipid homeostasis and regulating hepatocyte proliferation.
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