Sökning: onr:"swepub:oai:gup.ub.gu.se/314219" > ZMAT3 hypomethylati...
Fältnamn | Indikatorer | Metadata |
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000 | 05321naa a2200757 4500 | |
001 | oai:gup.ub.gu.se/314219 | |
003 | SwePub | |
008 | 240910s2022 | |||||||||||000 ||eng| | |
024 | 7 | a https://gup.ub.gu.se/publication/3142192 URI |
024 | 7 | a https://doi.org/10.1111/acel.135572 DOI |
040 | a (SwePub)gu | |
041 | a eng | |
042 | 9 SwePub | |
072 | 7 | a ref2 swepub-contenttype |
072 | 7 | a art2 swepub-publicationtype |
100 | 1 | a Spinelli, R.4 aut |
245 | 1 0 | a ZMAT3 hypomethylation contributes to early senescence of preadipocytes from healthy first-degree relatives of type 2 diabetics |
264 | c 2022-02-11 | |
264 | 1 | b Wiley,c 2022 |
520 | a Senescence of adipose precursor cells (APC) impairs adipogenesis, contributes to the age-related subcutaneous adipose tissue (SAT) dysfunction, and increases risk of type 2 diabetes (T2D). First-degree relatives of T2D individuals (FDR) feature restricted adipogenesis, reflecting the detrimental effects of APC senescence earlier in life and rendering FDR more vulnerable to T2D. Epigenetics may contribute to these abnormalities but the underlying mechanisms remain unclear. In previous methylome comparison in APC from FDR and individuals with no diabetes familiarity (CTRL), ZMAT3 emerged as one of the top-ranked senescence-related genes featuring hypomethylation in FDR and associated with T2D risk. Here, we investigated whether and how DNA methylation changes at ZMAT3 promote early APC senescence. APC from FDR individuals revealed increases in multiple senescence markers compared to CTRL. Senescence in these cells was accompanied by ZMAT3 hypomethylation, which caused ZMAT3 upregulation. Demethylation at this gene in CTRL APC led to increased ZMAT3 expression and premature senescence, which were reverted by ZMAT3 siRNA. Furthermore, ZMAT3 overexpression in APC determined senescence and activation of the p53/p21 pathway, as observed in FDR APC. Adipogenesis was also inhibited in ZMAT3-overexpressing APC. In FDR APC, rescue of ZMAT3 methylation through senolytic exposure simultaneously downregulated ZMAT3 expression and improved adipogenesis. Interestingly, in human SAT, aging and T2D were associated with significantly increased expression of both ZMAT3 and the P53 senescence marker. Thus, DNA hypomethylation causes ZMAT3 upregulation in FDR APC accompanied by acquisition of the senescence phenotype and impaired adipogenesis, which may contribute to FDR predisposition for T2D. | |
650 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Endokrinologi och diabetes0 (SwePub)302052 hsv//swe |
650 | 7 | a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Endocrinology and Diabetes0 (SwePub)302052 hsv//eng |
650 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Geriatrik0 (SwePub)302222 hsv//swe |
650 | 7 | a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Geriatrics0 (SwePub)302222 hsv//eng |
650 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Cell- och molekylärbiologi0 (SwePub)301082 hsv//swe |
650 | 7 | a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Cell and Molecular Biology0 (SwePub)301082 hsv//eng |
653 | a adipose precursor cells | |
653 | a aging | |
653 | a cellular senescence | |
653 | a DNA methylation | |
653 | a first-degree relatives of type 2 diabetics | |
653 | a senolytics | |
653 | a type 2 diabetes | |
653 | a ZMAT3 | |
653 | a impaired glucose-tolerance | |
653 | a cellular senescence | |
653 | a adipose-tissue | |
653 | a insulin | |
653 | a sensitivity | |
653 | a splicing regulator | |
653 | a tumor suppression | |
653 | a gene-expression | |
653 | a p53 | |
653 | a cells | |
653 | a wig-1 | |
653 | a Cell Biology | |
653 | a Geriatrics & Gerontology | |
700 | 1 | a Florese, P.4 aut |
700 | 1 | a Parrillo, L.4 aut |
700 | 1 | a Zatterale, F.4 aut |
700 | 1 | a Longo, M.4 aut |
700 | 1 | a D'Esposito, V.4 aut |
700 | 1 | a Desiderio, A.4 aut |
700 | 1 | a Nerstedt, Annika,d 1960u Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Institute of Medicine, Department of Molecular and Clinical Medicine4 aut0 (Swepub:gu)xneran |
700 | 1 | a Gustafson, Birgit,d 1951u Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Institute of Medicine, Department of Molecular and Clinical Medicine4 aut0 (Swepub:gu)xgustb |
700 | 1 | a Formisano, P.4 aut |
700 | 1 | a Miele, C.4 aut |
700 | 1 | a Raciti, G. A.4 aut |
700 | 1 | a Napoli, R.4 aut |
700 | 1 | a Smith, Ulf,d 1943u Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Institute of Medicine, Department of Molecular and Clinical Medicine4 aut0 (Swepub:gu)xsmiul |
700 | 1 | a Beguinot, F.4 aut |
710 | 2 | a Göteborgs universitetb Institutionen för medicin, avdelningen för molekylär och klinisk medicin4 org |
773 | 0 | t Aging Celld : Wileyg 21:3q 21:3x 1474-9718x 1474-9726 |
856 | 4 | u https://onlinelibrary.wiley.com/doi/pdfdirect/10.1111/acel.13557 |
856 | 4 8 | u https://gup.ub.gu.se/publication/314219 |
856 | 4 8 | u https://doi.org/10.1111/acel.13557 |
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