<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Nienhuser H</submitter><funding>Deutsche Forschungsgemeinschaft</funding><funding>NIDDK NIH HHS</funding><funding>Foundation for the National Institutes of Health</funding><funding>Deutsche Krebshilfe</funding><funding>NCI NIH HHS</funding><pagination>654-665</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10337481</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>70(4)</volume><pubmed_abstract>&lt;h4>Background and aims&lt;/h4>The gastric epithelium undergoes continuous turnover. Corpus epithelial stem cells located in the gastric isthmus serve as a source of tissue self-renewal. We recently identified the transcription factor Mist1 as a marker for this corpus stem cell population that can give rise to cancer. The aim here was to investigate the regulation of the Mist1+ stem cells in the response to gastric injury and inflammation.&lt;h4>Methods&lt;/h4>We used Mist1CreERT;R26-Tdtomato mice in two models of injury and inflammation: the acetic acid-induced ulcer and infection with &lt;i>Helicobacter felis&lt;/i>. We analysed lineage tracing at both early (7 to 30 days) and late (30 to 90 days) time points. Mist1CreERT;R26-Tdtomato;Lgr5DTR-eGFP mice were used to ablate the corpus basal Lgr5+ cell po</pubmed_abstract><journal>Gut</journal><pubmed_title>Mist1+ gastric isthmus stem cells are regulated by Wnt5a and expand in response to injury and inflammation in mice.</pubmed_title><pmcid>PMC10337481</pmcid><funding_grant_id>5UO1DK103155</funding_grant_id><funding_grant_id>R35 CA210088</funding_grant_id><funding_grant_id>NI1810/1-1</funding_grant_id><funding_grant_id>R01 CA224428</funding_grant_id><funding_grant_id>R37 DK052778</funding_grant_id><funding_grant_id>U01 DK103155</funding_grant_id><funding_grant_id>U01 DK085532</funding_grant_id><funding_grant_id>70111870</funding_grant_id><funding_grant_id>R35CA210088</funding_grant_id><funding_grant_id>U24 DK085532</funding_grant_id><funding_grant_id>P30 CA013696</funding_grant_id><funding_grant_id>5R37DK052778</funding_grant_id><pubmed_authors>Kim W</pubmed_authors><pubmed_authors>Middelhoff M</pubmed_authors><pubmed_authors>Nienhuser H</pubmed_authors><pubmed_authors>Valenti G</pubmed_authors><pubmed_authors>Malagola E</pubmed_authors><pubmed_authors>Der CJ</pubmed_authors><pubmed_authors>Bass A</pubmed_authors><pubmed_authors>Wang TC</pubmed_authors><pubmed_authors>Ruan T</pubmed_authors><pubmed_authors>Hayakawa Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Mist1+ gastric isthmus stem cells are regulated by Wnt5a and expand in response to injury and inflammation in mice.</name><description>&lt;h4>Background and aims&lt;/h4>The gastric epithelium undergoes continuous turnover. Corpus epithelial stem cells located in the gastric isthmus serve as a source of tissue self-renewal. We recently identified the transcription factor Mist1 as a marker for this corpus stem cell population that can give rise to cancer. The aim here was to investigate the regulation of the Mist1+ stem cells in the response to gastric injury and inflammation.&lt;h4>Methods&lt;/h4>We used Mist1CreERT;R26-Tdtomato mice in two models of injury and inflammation: the acetic acid-induced ulcer and infection with &lt;i>Helicobacter felis&lt;/i>. We analysed lineage tracing at both early (7 to 30 days) and late (30 to 90 days) time points. Mist1CreERT;R26-Tdtomato;Lgr5DTR-eGFP mice were used to ablate the corpus basal Lgr5+ cell po</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Apr</publication><modification>2025-04-04T13:52:35.861Z</modification><creation>2025-04-04T13:52:35.861Z</creation></dates><accession>S-EPMC10337481</accession><cross_references><pubmed>32709613</pubmed><doi>10.1136/gutjnl-2020-320742</doi></cross_references></HashMap>