Abstract
Diethoxycarbonyl dihydrocollidine (DDC) diet induces significant bile duct and hepatocyte injury mimicking human cholestatic liver disease. Following DDC injury, repair is often observed via ductular proliferation of expansion of biliary markers in the hepatocytes. However, the role of Wnt secretion by hepatocytes during DDC injury and repair remains elusive. Alb‐Cre+/‐;Wlsflox/flox mice, which lack the ability to secrete Wnt from hepatocytes, were exposed to DDC diet, and pathological characteristics were compared between wild type (WT) and hepatocyte‐specific Wls knock out (KO) mice. Expression of Wnt7A, Wnt7B and Wnt10B were induced by DDC treatment in WT mice. WT had more abundant A6 positive ductular cells indicating higher ductular proliferation as compared to KO. WT showed more CD45+ cells and collagen deposits than KO. KO showed higher serum total bilirubin level, and poor survival, resulting in worse prognosis than WT. Wnt secreted by hepatocytes might be crucial factor to induce ductular proliferation. This response is important repair mechanism after DDC injury.
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