<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Dey S</submitter><funding>NCATS NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>Indiana Clinical and Translational Sciences Institute</funding><funding>NCI NIH HHS</funding><funding>Indiana University Simon Cancer Center</funding><pagination>e149539</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8525644</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>6(19)</volume><pubmed_abstract>MicroRNA-29 (miR-29) is a critical regulator of fibroinflammatory processes in human diseases. In this study, we found a decrease in miR-29a in experimental and human chronic pancreatitis, leading us to investigate the regulatory role of the miR-29a/b1 cluster in acute pancreatitis (AP) utilizing a conditional miR-29a/b1-KO mouse model. miR-29a/b1-sufficient (WT) and -deficient (KO) mice were administered supramaximal caerulein to induce AP and characterized at different time points, utilizing an array of IHC and biochemical analyses for AP parameters. In caerulein-induced WT mice, miR-29a remained dramatically downregulated at injury. Despite high-inflammatory milieu, fibrosis, and parenchymal disarray in the WT mice during early AP, the pancreata fully restored during recovery. miR-29a/b</pubmed_abstract><journal>JCI insight</journal><pubmed_title>Loss of miR-29a/b1 promotes inflammation and fibrosis in acute pancreatitis.</pubmed_title><pmcid>PMC8525644</pmcid><funding_grant_id>U01 DK108323</funding_grant_id><funding_grant_id>P30CA082709</funding_grant_id><funding_grant_id>P30 CA082709</funding_grant_id><funding_grant_id>UL1TR001108</funding_grant_id><funding_grant_id>UL1 TR001108</funding_grant_id><pubmed_authors>Easler JJ</pubmed_authors><pubmed_authors>Pandol S</pubmed_authors><pubmed_authors>Dey S</pubmed_authors><pubmed_authors>Kota J</pubmed_authors><pubmed_authors>Udari LM</pubmed_authors><pubmed_authors>Kwon JJ</pubmed_authors><pubmed_authors>Fogel EL</pubmed_authors><pubmed_authors>RiveraHernandez P</pubmed_authors><pubmed_authors>Willis B</pubmed_authors></additional><is_claimable>false</is_claimable><name>Loss of miR-29a/b1 promotes inflammation and fibrosis in acute pancreatitis.</name><description>MicroRNA-29 (miR-29) is a critical regulator of fibroinflammatory processes in human diseases. In this study, we found a decrease in miR-29a in experimental and human chronic pancreatitis, leading us to investigate the regulatory role of the miR-29a/b1 cluster in acute pancreatitis (AP) utilizing a conditional miR-29a/b1-KO mouse model. miR-29a/b1-sufficient (WT) and -deficient (KO) mice were administered supramaximal caerulein to induce AP and characterized at different time points, utilizing an array of IHC and biochemical analyses for AP parameters. In caerulein-induced WT mice, miR-29a remained dramatically downregulated at injury. Despite high-inflammatory milieu, fibrosis, and parenchymal disarray in the WT mice during early AP, the pancreata fully restored during recovery. miR-29a/b</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Oct</publication><modification>2026-05-08T15:50:44.253Z</modification><creation>2025-02-19T00:03:23.011Z</creation></dates><accession>S-EPMC8525644</accession><cross_references><pubmed>34464354</pubmed><doi>10.1172/jci.insight.149539</doi></cross_references></HashMap>