Liver progenitor cells are necessary for repair in chronic liver disease since the remaining hepatocytes cannot replicate. However, liver progenitor cell numbers also correlate with disease severity and hepatocellular carcinoma risk. Thus, the progenitor cell response in diseased liver may be regulated to optimise liver regeneration and minimise likelihood of tumorigenesis. How this is achieved is currently unknown. Human and mouse diseased liver contain two subpopulations of macrophages with different ontogenetic origins; prenatal yolk sac-derived Kupffer cells (KCs), and peripheral blood monocyte-derived macrophages (MDMs). We examined the individual role(s) of KCs and MDMs in the induction of LPC proliferation using clodronate liposome deletion of KCs and adoptive transfer of monocytes, respectively, in the choline-deficient, ethionine-supplemented diet model of liver injury and regeneration. Clodronate liposome treatment reduced initial liver monocyte numbers together with the induction of injury and LPC proliferation. Adoptive transfer of monocytes increased induction of liver injury, LPC proliferation, and TNFα production.
Kupffer cells control the initial accumulation of monocyte-derived macrophages. These infiltrating monocytes are in turn responsible for the induction of liver injury, the increase in TNFα, and the subsequent proliferation of liver progenitor cells. This article is protected by copyright. All rights reserved.
This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 23 October 2015.
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#15,739,529
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