{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cataldi S"],"funding":["European Foundation for the Study of Diabetes","Ministero dell’Istruzione, dell’Università e della Ricerca"],"pagination":["42"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8750445"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(1)"],"pubmed_abstract":["Low-grade chronic inflammation and reduced differentiation capacity are hallmarks of hypertrophic adipose tissue (AT) and key contributors of insulin resistance. We identified PPARGΔ5 as a dominant-negative splicing isoform overexpressed in the AT of obese/diabetic patients able to impair adipocyte differentiation and PPARγ activity in hypertrophic adipocytes. Herein, we investigate the impact of macrophage-secreted pro-inflammatory factors on PPARG splicing, focusing on PPARGΔ5. We report that the epididymal AT of LPS-treated mice displays increased PpargΔ5/cPparg ratio and reduced expression of Pparg-regulated genes. Interestingly, pro-inflammatory factors secreted from murine and human pro-inflammatory macrophages enhance the PPARGΔ5/cPPARG ratio in exposed adipogenic precursors. TNFα i"],"journal":["Cells"],"pubmed_title":["TNFα Mediates Inflammation-Induced Effects on PPARG Splicing in Adipose Tissue and Mesenchymal Precursor Cells."],"pmcid":["PMC8750445"],"funding_grant_id":["Boehringer Ingelheim European Research Programme in Microvascular Complications of Diabetes","PON Ricerca e Innovazione 2014–2020, PON Ars01_01270 “Innovative Device For SHAping the Risk of Diabetes” (IDF SHARID)"],"pubmed_authors":["Melillo D","Tanti JF","Mucel I","Italiani P","Aprile M","Cormont M","Bluher M","Costa V","Cataldi S","Ciccodicola A","Giorgetti-Peraldi S"],"additional_accession":[]},"is_claimable":false,"name":"TNFα Mediates Inflammation-Induced Effects on PPARG Splicing in Adipose Tissue and Mesenchymal Precursor Cells.","description":"Low-grade chronic inflammation and reduced differentiation capacity are hallmarks of hypertrophic adipose tissue (AT) and key contributors of insulin resistance. We identified PPARGΔ5 as a dominant-negative splicing isoform overexpressed in the AT of obese/diabetic patients able to impair adipocyte differentiation and PPARγ activity in hypertrophic adipocytes. Herein, we investigate the impact of macrophage-secreted pro-inflammatory factors on PPARG splicing, focusing on PPARGΔ5. We report that the epididymal AT of LPS-treated mice displays increased PpargΔ5/cPparg ratio and reduced expression of Pparg-regulated genes. Interestingly, pro-inflammatory factors secreted from murine and human pro-inflammatory macrophages enhance the PPARGΔ5/cPPARG ratio in exposed adipogenic precursors. TNFα i","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Dec","modification":"2025-06-01T12:06:37.386Z","creation":"2025-06-01T12:06:37.386Z"},"accession":"S-EPMC8750445","cross_references":{"pubmed":["35011604"],"doi":["10.3390/cells11010042"]}}