{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Dey S"],"funding":["NCATS NIH HHS","NIDDK NIH HHS","Indiana Clinical and Translational Sciences Institute","NCI NIH HHS","Indiana University Simon Cancer Center"],"pagination":["e149539"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8525644"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["6(19)"],"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"],"journal":["JCI insight"],"pubmed_title":["Loss of miR-29a/b1 promotes inflammation and fibrosis in acute pancreatitis."],"pmcid":["PMC8525644"],"funding_grant_id":["U01 DK108323","P30CA082709","P30 CA082709","UL1TR001108","UL1 TR001108"],"pubmed_authors":["Easler JJ","Pandol S","Dey S","Kota J","Udari LM","Kwon JJ","Fogel EL","RiveraHernandez P","Willis B"],"additional_accession":[]},"is_claimable":false,"name":"Loss of miR-29a/b1 promotes inflammation and fibrosis in acute pancreatitis.","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","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Oct","modification":"2026-05-08T15:50:44.253Z","creation":"2025-02-19T00:03:23.011Z"},"accession":"S-EPMC8525644","cross_references":{"pubmed":["34464354"],"doi":["10.1172/jci.insight.149539"]}}