<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>14(17)</volume><submitter>Yamamoto T</submitter><pubmed_abstract>The mechanisms involved in the regeneration of biliary epithelial cells (BECs) after liver injury remain unclear. In this study, we employed KRT19Cre&lt;sup>ERT&lt;/sup>/LSL-tdTomato (KT) mice and KT/TFF1KO mice to clarify the regeneration and cell fate of BECs via lineage tracing. Tamoxifen (TAM) was administered to the mice to label cytokeratin 19 (CK19)-positive BECs. The mice were subsequently fed a choline-deficient, ethionine-supplemented (CDE) diet for four weeks, after which the mouse livers were analyzed. Whereas the proportion of tdTomato&lt;sup>+&lt;/sup> cells in CK19-positive BECs decreased in the KT mice, it remained high in the KT/TFF1KO mice. Then, we analyzed hepatic progenitor cells (HPCs), the possible source of BECs. Although tdTomato-labeled HPCs were rarely found in the pretreatm</pubmed_abstract><journal>Cells</journal><pagination>1323</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12428306</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Dedifferentiation-Dependent Regeneration of the Biliary Ductal Epithelium in Response to Hepatic Injury in TFF1-Deficient Mice.</pubmed_title><pmcid>PMC12428306</pmcid><pubmed_authors>Mizuno T</pubmed_authors><pubmed_authors>Ebata T</pubmed_authors><pubmed_authors>Kokuryo T</pubmed_authors><pubmed_authors>Sunagawa M</pubmed_authors><pubmed_authors>Yokoyama Y</pubmed_authors><pubmed_authors>Baba T</pubmed_authors><pubmed_authors>Yamamoto T</pubmed_authors><pubmed_authors>Onoe S</pubmed_authors><pubmed_authors>Yamaguchi J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Dedifferentiation-Dependent Regeneration of the Biliary Ductal Epithelium in Response to Hepatic Injury in TFF1-Deficient Mice.</name><description>The mechanisms involved in the regeneration of biliary epithelial cells (BECs) after liver injury remain unclear. In this study, we employed KRT19Cre&lt;sup>ERT&lt;/sup>/LSL-tdTomato (KT) mice and KT/TFF1KO mice to clarify the regeneration and cell fate of BECs via lineage tracing. Tamoxifen (TAM) was administered to the mice to label cytokeratin 19 (CK19)-positive BECs. The mice were subsequently fed a choline-deficient, ethionine-supplemented (CDE) diet for four weeks, after which the mouse livers were analyzed. Whereas the proportion of tdTomato&lt;sup>+&lt;/sup> cells in CK19-positive BECs decreased in the KT mice, it remained high in the KT/TFF1KO mice. Then, we analyzed hepatic progenitor cells (HPCs), the possible source of BECs. Although tdTomato-labeled HPCs were rarely found in the pretreatm</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Aug</publication><modification>2026-04-08T19:11:08.763Z</modification><creation>2026-04-08T12:02:06.72Z</creation></dates><accession>S-EPMC12428306</accession><cross_references><pubmed>40940735</pubmed><doi>10.3390/cells14171323</doi></cross_references></HashMap>