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WNT7B Regulates Cholangiocyte Proliferation and Function During Murine Cholestasis by Kosar, Karis (author);Cornuet, Pamela (author);Singh, Sucha (author);Lee, Elizabeth (author);Liu, Silvia (author);Gayden, Jenesis (author);Sato, Toshifumi (author);Freyberg, Zachary (author);Arteel, Gavin (author);Nejak‐Bowen, Kari (author) is a Medicine article available to read on EtoBox.

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We previously identified an up‐regulation of specific Wnt proteins in the cholangiocyte compartment during cholestatic liver injury and found that mice lacking Wnt secretion from hepatocytes and cholangiocytes showed fewer proliferating cholangiocytes and high mortality in response to a 3,5‐diethoxycarbonyl‐1,4‐dihydrocollidine (DDC) diet, a murine model of primary sclerosing cholangitis. __In vitro__ studies demonstrated that Wnt7b, one of the Wnts up‐regulated during cholestasis, induces proliferation of cholangiocytes in an autocrine manner and increases secretion of proinflammatory cytokines. We hypothesized that loss of Wnt7b may exacerbate some of the complications of cholangiopathies by decreasing the ability of bile ducts to induce repair. Wnt7b‐flox mice were bred with Krt19‐cre mice to deplete Wnt7b expression in only cholangiocytes (CC) or with albumin‐Cre mice to delete Wnt7b expression in both hepatocytes and cholangiocytes (HC + CC). These mice were placed on a DDC diet for 1 month then killed for evaluation. Contrary to our expectations, we found that mice lacking Wnt7b from CC and HC + CC compartments had improved biliary injury, decreased cellular senescence, and l

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Author

Kosar, Karis (author);Cornuet, Pamela (author);Singh, Sucha (author);Lee, Elizabeth (author);Liu, Silvia (author);Gayden, Jenesis (author);Sato, Toshifumi (author);Freyberg, Zachary (author);Arteel, Gavin (author);Nejak‐Bowen, Kari (author)

Publisher

Ovid Technologies (Wolters Kluwer Health)

Published

2021

Language

EN

Field

Medicine (Health Sciences)