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NADPH oxidase 4 in mouse β cells participates in inflammation on chronic nutrient overload
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SYSNO ASEP 0582386 Druh ASEP J - Článek v odborném periodiku Zařazení RIV J - Článek v odborném periodiku Poddruh J Článek ve WOS Název NADPH oxidase 4 in mouse β cells participates in inflammation on chronic nutrient overload Tvůrce(i) Holendová, Blanka (FGU-C) RID, ORCID, SAI
Benáková, Štěpánka (FGU-C) ORCID
Křivonosková, Monika (FGU-C) ORCID
Pavluch, Vojtěch (FGU-C) RID, ORCID
Tauber, Jan (FGU-C) RID, ORCID
Gabrielová, E. (CZ)
Ježek, Petr (FGU-C) RID, ORCID
Plecitá-Hlavatá, Lydie (FGU-C) RID, ORCIDZdroj.dok. Obesity - ISSN 1930-7381
Roč. 32, č. 2 (2024), s. 339-351Poč.str. 13 s. Jazyk dok. eng - angličtina Země vyd. US - Spojené státy americké Klíč. slova beta-cells ; inflammation ; interleukin-1 ; IL-1 Obor OECD Endocrinology and metabolism (including diabetes, hormones) CEP GA21-01205S GA ČR - Grantová agentura ČR GA22-11439S GA ČR - Grantová agentura ČR LX22NPO5104 GA MŠMT - Ministerstvo školství, mládeže a tělovýchovy Výzkumná infrastruktura CCP II - 90126 - Ústav molekulární genetiky AV ČR, v. v. i. Způsob publikování Open access Institucionální podpora FGU-C - RVO:67985823 UT WOS 001122685600001 EID SCOPUS 85179336490 DOI 10.1002/oby.23956 Anotace Objective:By exposing mice carrying a deletion of NADPH oxidase isoform 4, NOX4, specifically in pancreatic β cells (βNOX4−/−) to nutrient excess stimulated by a high-fat diet (HFD), this study aimed to elucidate the role of β-cell redox status in the development of meta-inflammation within the diabetic phenotype.Methods:The authors performed basic phenotyping of βNOX4−/− mice on HFD involving insulin and glycemic analyses, histochemistry of adipocytes, indirect calorimetry, and cytokine analyses. To characterize local inflammation, the study used caspase-1 activity assay, interleukin-1β immunochemistry, and real-time polymerase chain reaction during coculturing of β cells with macrophages.Results:The phenotype of βNOX4−/− mice on HFD was not associated with hyperinsulinemia and hyperglycemia but showed accumulation of excessive lipids in epididymal fat and β cells. Surprisingly, mice showed significantly reduced systemic inflammation. Decreased interleukin-1β protein levels and downregulated NLRP3-inflammasome activity were observed on chronic glucose overload in βNOX4−/− isolated islets and NOX4-silenced INS1-E cells resulting in attenuated proinflammatory polarization of macrophages/monocytes in vitro and in situ and reduced local islet inflammation.Conclusions:Experimental evidence suggests that NOX4 pro-oxidant activity in β cells is involved in NLRP3-inflammasome activation during chronic nutrient overload and participates in local inflammatory signaling and perhaps toward peripheral tissues, contributing to a diabetic inflammatory phenotype. Pracoviště Fyziologický ústav Kontakt Lucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400 Rok sběru 2025 Elektronická adresa https://doi.org/10.1002/oby.23956
Počet záznamů: 1