{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Mukherjee K"],"funding":["NIDDK NIH HHS","U.S. Department of Health & Human Services | National Institutes of Health","U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases"],"pagination":["2422"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9065033"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(1)"],"pubmed_abstract":["Chronic kidney diseases and acute kidney injury are mechanistically distinct kidney diseases. While chronic kidney diseases are associated with podocyte injury, acute kidney injury affects renal tubular epithelial cells. Despite these differences, a cardinal feature of both acute and chronic kidney diseases is dysregulated actin cytoskeleton. We have shown that pharmacological activation of GTPase dynamin ameliorates podocyte injury in murine models of chronic kidney diseases by promoting actin polymerization. Here we establish dynamin's role in modulating stiffness and polarity of renal tubular epithelial cells by crosslinking actin filaments into branched networks. Activation of dynamin's crosslinking capability by a small molecule agonist stabilizes the actomyosin cortex of the apical m"],"journal":["Nature communications"],"pubmed_title":["Simultaneous stabilization of actin cytoskeleton in multiple nephron-specific cells protects the kidney from diverse injury."],"pmcid":["PMC9065033"],"funding_grant_id":["GM73165","R01 DK093773","CA227747","R01 DK087985","R01 DK084195"],"pubmed_authors":["Bouley R","Sudhini YR","Gupta V","Sever S","Samelko B","Brown D","Collins A","Brinkkoetter PT","Mukherjee K","Reiser J","Gu C","Pedro BP","Hagmann H","Mettlen M","Wang X","Altintas MM","Bane SL"],"additional_accession":[]},"is_claimable":false,"name":"Simultaneous stabilization of actin cytoskeleton in multiple nephron-specific cells protects the kidney from diverse injury.","description":"Chronic kidney diseases and acute kidney injury are mechanistically distinct kidney diseases. While chronic kidney diseases are associated with podocyte injury, acute kidney injury affects renal tubular epithelial cells. Despite these differences, a cardinal feature of both acute and chronic kidney diseases is dysregulated actin cytoskeleton. We have shown that pharmacological activation of GTPase dynamin ameliorates podocyte injury in murine models of chronic kidney diseases by promoting actin polymerization. Here we establish dynamin's role in modulating stiffness and polarity of renal tubular epithelial cells by crosslinking actin filaments into branched networks. Activation of dynamin's crosslinking capability by a small molecule agonist stabilizes the actomyosin cortex of the apical m","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 May","modification":"2025-06-01T12:13:17.79Z","creation":"2025-06-01T12:13:17.79Z"},"accession":"S-EPMC9065033","cross_references":{"pubmed":["35504916"],"doi":["10.1038/s41467-022-30101-4"]}}