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EZH2 inhibitors promote β-like cell regeneration in young and adult type 1 diabetes donors

Signal Transduction and Targeted Therapy 2024年第2期9卷 679-692页

作者： Keith Al-Hasani Safiya Naina Marikar Harikrishnan Kaipananickal Scott Maxwell Jun Okabe Ishant Khurana thomas Karagiannis Julia J.Liang Lina Mariana thomas loudovaris thomas Kay Assam El-Osta Epigenetics in Human Health and Disease Program Baker Heart and Diabetes Institute75 Commercial RoadMelbourne 3004 VICAustralia Department of Diabetes Central Clinical SchoolMonash UniversityMelbourne 3004 VICAustralia Epigenetics in Human Health and Disease Laboratory Central Clinical SchoolMonash UniversityMelbourne 3004 VICAustralia School of Science STEM CollegeRMIT UniversityMelbourne 3001 VICAustralia Immunology and Diabetes Unit St Vincent’s Institute of Medical ResearchFitzroy 3065 VICAustralia Department of Medicine and Therapeutics The Chinese University of Hong KongSha TinHong Kong SAR Hong Kong Institute of Diabetes and Obesity Prince of Wales HospitalThe Chinese University of Hong Kong3/F Lui Che Woo Clinical Sciences Building30-32-Ngan Shing StreetSha TinHong Kong SAR Li Ka Shing Institute of Health Sciences The Chinese University of Hong KongSha TinHong Kong SAR Biomedical Laboratory Science Department of TechnologyFaculty of HealthUniversity College CopenhagenCopenhagenDenmark

β-cells are a type of endocrine cell found in pancreatic islets that synthesize,store and release *** type 1 diabetes(T1D),T-cells of the immune system selectively destroy the insulin-producingβ-*** of these cells leads to a lifelong dependence on exogenous insulin administration for ***,there is an urgent need to identify novel therapies that stimulateβ-cell growth and induceβ-cell *** and others have shown that pancreatic ductal progenitor cells are a promising source for regeneratingβ-cells for T1D owing to their inherent differentiation *** transcriptional suppression is refractory to exocrine reaction and tightly controls the regenerative potential by the EZH2 *** the present study,we show that transient stimulation of exocrine cells,derived from juvenile and adult T1D donors to the FDAapproved EZH2 inhibitors GSK126 and Tazemetostat(Taz)influence a phenotypic shift towards aβ-like cell *** transition from repressed to permissive chromatin states are dependent on bivalent H3K27me3 and H3K4me3 chromatin *** EZH2 is fundamental toβ-cell regenerative *** pancreatic ductal cells exhibit insulin production and secretion in response to a physiological glucose challenge ex *** pre-clinical studies underscore the potential of small molecule inhibitors as novel modulators of ductal progenitor differentiation and a promising new approach for the restoration ofβ-like cell function.

关键词： EZH2 struction inhibitors

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Inhibition of pancreatic EZH2 restores progenitor insulin in T1D donor

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Signal Transduction and Targeted Therapy 2022年第8期7卷 3045-3053页

作者： Keith Al-Hasani Ishant Khurana Lina Mariana thomas loudovaris Scott Maxwell K.N.Harikrishnan Jun Okabe Mark ECooper Assam El-Osta Department of Diabetes Central Clinical SchoolMonash UniversityMelbourneVictoria 3004Australia Epigenetics in Human Health and Disease Laboratory Central Clinical SchoolMonash UniversityMelbourneVictoria 3004Australia Immunology and Diabetes Unit St Vincent’s Institute of Medical ResearchFitzroyVictoriaAustralia Department of Clinical Pathology The University of MelbourneParkvilleVictoriaAustralia Department of Medicine and Therapeutics The Chinese University of Hong KongSha TinHong Kong SAR Hong Kong Institute of Diabetes and Obesity Prince of Wales HospitalThe Chinese University of Hong Kong3/F Lui Che Woo Clinical Sciences Building30-32 Ngan Shing StreetSha TinHong Kong SAR Li Ka Shing Institute of Health Sciences The Chinese University of Hong KongSha TinHong Kong SAR Faculty of Health Department of TechnologyBiomedical Laboratory ScienceUniversity College CopenhagenCopenhagenDenmark

Type 1 diabetes(T1D)is an autoimmune disease that selectively destroys insulin-producingβ-cells in the *** unmet need in diabetes management,current therapy is focussed on *** the reprogramming of progenitor cells into functional insulin-producingβ-cells has also been proposed this remains controversial and poorly *** challenge is determining why default transcriptional suppression is refractory to exocrine *** the death of a 13-year-old girl with established insulin-dependent T1D,pancreatic cells were harvested in an effort to restore and understand exocrine *** pancreas showed classic silencing ofβ-cell progenitor genes with barely detectable insulin(Ins)***126,a highly selective inhibitor of EZH2 methyltransferase activity influenced H3K27me3 chromatin content and transcriptional control resulting in the expression of coreβ-cell markers and ductal progenitor ***126 also reinstated Ins gene expression despite absoluteβ-cell *** studies show the refractory nature of chromatin characterises exocrine suppression influencingβ-cell *** regeneration studies are warranted to determine if the approach of this n-of-1 study generalises to a broader T1D population.

关键词： EZH2 progenitor donor

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