<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Leibing T</submitter><funding>Deutsche Forschungsgemeinschaft</funding><pagination>707-722</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6099291</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>68(2)</volume><pubmed_abstract>Postnatal liver development is characterized by hepatocyte growth, proliferation, and functional maturation. Notably, canonical Wnt signaling in hepatocytes has been identified as an important regulator of final adult liver size and metabolic liver zonation. The cellular origin of Wnt ligands responsible for homeostatic liver/body weight ratio (LW/BW) remained unclear, which was also attributable to a lack of suitable endothelial Cre driver mice. To comprehensively analyze the effects of hepatic angiocrine Wnt signaling on liver development and metabolic functions, we used endothelial subtype-specific Stab2-Cre driver mice to delete Wls from hepatic endothelial cells (HECs). The resultant Stab2-Cre&lt;sup>tg/wt&lt;/sup> ;Wls&lt;sup>fl/fl&lt;/sup> (Wls-HECKO) mice were viable, but showed a significantl</pubmed_abstract><journal>Hepatology (Baltimore, Md.)</journal><pubmed_title>Angiocrine Wnt signaling controls liver growth and metabolic maturation in mice.</pubmed_title><pmcid>PMC6099291</pmcid><funding_grant_id>DFG INST 91027/10-1 FUGG</funding_grant_id><funding_grant_id>GRK2099/RTG2099, project 7</funding_grant_id><funding_grant_id>DFG INST 91027/9-1 FUGG</funding_grant_id><funding_grant_id>SFB-TR23, project B1</funding_grant_id><pubmed_authors>Geraud C</pubmed_authors><pubmed_authors>Zierow J</pubmed_authors><pubmed_authors>Leibing T</pubmed_authors><pubmed_authors>Schledzewski K</pubmed_authors><pubmed_authors>Okun JG</pubmed_authors><pubmed_authors>Goerdt S</pubmed_authors><pubmed_authors>Olsavszky V</pubmed_authors><pubmed_authors>Augustin HG</pubmed_authors><pubmed_authors>Koch PS</pubmed_authors><pubmed_authors>Boutros M</pubmed_authors><pubmed_authors>Wohlfeil SA</pubmed_authors><pubmed_authors>Augustin I</pubmed_authors><pubmed_authors>Langhans CD</pubmed_authors></additional><is_claimable>false</is_claimable><name>Angiocrine Wnt signaling controls liver growth and metabolic maturation in mice.</name><description>Postnatal liver development is characterized by hepatocyte growth, proliferation, and functional maturation. Notably, canonical Wnt signaling in hepatocytes has been identified as an important regulator of final adult liver size and metabolic liver zonation. The cellular origin of Wnt ligands responsible for homeostatic liver/body weight ratio (LW/BW) remained unclear, which was also attributable to a lack of suitable endothelial Cre driver mice. To comprehensively analyze the effects of hepatic angiocrine Wnt signaling on liver development and metabolic functions, we used endothelial subtype-specific Stab2-Cre driver mice to delete Wls from hepatic endothelial cells (HECs). The resultant Stab2-Cre&lt;sup>tg/wt&lt;/sup> ;Wls&lt;sup>fl/fl&lt;/sup> (Wls-HECKO) mice were viable, but showed a significantl</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Aug</publication><modification>2026-05-05T20:38:03.99Z</modification><creation>2019-03-26T23:52:24Z</creation></dates><accession>S-EPMC6099291</accession><cross_references><pubmed>29059455</pubmed><doi>10.1002/hep.29613</doi></cross_references></HashMap>