The Activation of the NF-κB Pathway in Human Adipose-Derived Stem Cells Alters the Deposition of Epigenetic Marks on H3K27 and Is Modulated by Fish Oil DOI Creative Commons
Jussara de Jesus Simão, Andressa França de Sousa Bispo, Victor Tadeu Gonçalves Plata

и другие.

Life, Год журнала: 2024, Номер 14(12), С. 1653 - 1653

Опубликована: Дек. 12, 2024

Background: Chronic low-grade inflammation in obesity is linked to white adipose tissue (WAT) dysfunction. Plasma lipopolysaccharide (LPS) activates Toll-like receptor 4 (TLR4), triggering NF-κB and worsening these disturbances. Previously, we showed that histone H3 lysine 27 (H3K27) epigenetic modifications affect WAT gene expression high-fat-diet mice, identifying key pathways adipose-derived stem cells (ASCs). This study explores whether influences H3K27 modifiers human ASCs evaluates fish oil (FO) as a modulator. Methods: Human visceral were stimulated with LPS treated FO enriched eicosapentaenoic acid (EPA). Flow cytometry, PCR array, RT-PCR, Western blot assays used. Results: increased activity, elevating KDM6B demethylase levels acetylation. These LPS-stimulated associated persistent changes the of genes involved adipogenesis, metabolic regulation, inflammation, even after removal cell differentiation. mitigated effects, reducing acetylation promoting methylation. Conclusions: demonstrates potential modulating inflammation-induced preserving adipocyte function.

Язык: Английский

Fish Oil Supplementation Mitigates High-Fat Diet-Induced Obesity: Exploring Epigenetic Modulation and Genes Associated with Adipose Tissue Dysfunction in Mice DOI Creative Commons
Jussara de Jesus Simão,

A Bispo,

Victor Tadeu Gonçalves Plata

и другие.

Pharmaceuticals, Год журнала: 2024, Номер 17(7), С. 861 - 861

Опубликована: Июль 1, 2024

This study investigated the effects of fish oil (FO) treatment, particularly enriched with eicosapentaenoic acid (EPA), on obesity induced by a high-fat diet (HFD) in mice. The investigation focused elucidating impact FO epigenetic modifications white adipose tissue (WAT) and involvement adipose-derived stem cells (ASCs). C57BL/6j mice were divided into two groups: control HFD for 16 weeks. In last 8 weeks, group was subdivided + (treated FO). WAT removed RNA protein extraction, while ASCs isolated, cultured, treated leptin. All samples analyzed using functional genomics tools, including PCR-array, RT-PCR, Western Blot assays. Mice receiving an displayed increased body mass, fat accumulation, altered gene expression associated inflammation dysfunction. supplementation attenuated these effects, potential protective role against HFD-induced obesity. Analysis H3K27 revealed changes histone, which partially reversed treatment. further explored leptin signaling ASCs, suggesting mechanism ASC dysfunction obesity-rich environment WAT. Overall, demonstrated efficacy mitigating obesity, influencing molecular pathways, shedding light

Язык: Английский

Процитировано

6
SUV39H1 alleviates MAFLD through inhibition of the FABPs/CEPT1 signaling pathway DOI Creative Commons

Yi Sun,

Changyuan Wang, Yang Wang

и другие.

Research Square (Research Square), Год журнала: 2025, Номер unknown

Опубликована: Янв. 10, 2025

Abstract Background Epigenetics modification has emerged as a potential mechanism of action for MAFLD. The histone methylase SUV39H1 is key epigenetic transcription factor that regulates adipogenesis and inflammation, but its role in MAFLD progression remains largely unknown. Methods In this study, the high fat diet (HFD) induced mice palmitic acid (PA) primary mouse hepatocytes were adopted to investigate effects mechanisms on Point mutation knockdown SET domain PA-stimulated AML12 cells high-fat fed confirm function RNA–sequencing was used screen downstream genes affected by overexpression PA-induced cells. functional relationship between FABPs elucidated CHIP, DNA Pull Down dual-luciferase reporter assays. Results could attenuate affecting lipid metabolism, suppressing inflammation insulin resistance. And proved be mediating vivo vitro. Further studies revealed or CEPT1, accelerate disorder metabolism Meanwhile, FABP promote CEPT1 expression. Histone methylation promoters inhibit MAFLD.In addition, derived from aggravate promoting M1 polarization macrophages. Conclusion alleviates through inhibition FABPs/CEPT1 signaling pathway.

Язык: Английский

Процитировано

0
WITHDRAWN: SUV39H1 alleviates MAFLD through inhibition of the FABPs/CEPT1 signaling pathway DOI Creative Commons

Yi Sun,

Changyuan Wang, Yang Wang

и другие.

Research Square (Research Square), Год журнала: 2025, Номер unknown

Опубликована: Янв. 13, 2025

Abstract The full text of this preprint has been withdrawn, as it was submitted in error. Therefore, the authors do not wish work to be cited a reference. Questions should directed corresponding author.

Язык: Английский

Процитировано

0
The Activation of the NF-κB Pathway in Human Adipose-Derived Stem Cells Alters the Deposition of Epigenetic Marks on H3K27 and Is Modulated by Fish Oil DOI Creative Commons
Jussara de Jesus Simão, Andressa França de Sousa Bispo, Victor Tadeu Gonçalves Plata

и другие.

Life, Год журнала: 2024, Номер 14(12), С. 1653 - 1653

Опубликована: Дек. 12, 2024

Background: Chronic low-grade inflammation in obesity is linked to white adipose tissue (WAT) dysfunction. Plasma lipopolysaccharide (LPS) activates Toll-like receptor 4 (TLR4), triggering NF-κB and worsening these disturbances. Previously, we showed that histone H3 lysine 27 (H3K27) epigenetic modifications affect WAT gene expression high-fat-diet mice, identifying key pathways adipose-derived stem cells (ASCs). This study explores whether influences H3K27 modifiers human ASCs evaluates fish oil (FO) as a modulator. Methods: Human visceral were stimulated with LPS treated FO enriched eicosapentaenoic acid (EPA). Flow cytometry, PCR array, RT-PCR, Western blot assays used. Results: increased activity, elevating KDM6B demethylase levels acetylation. These LPS-stimulated associated persistent changes the of genes involved adipogenesis, metabolic regulation, inflammation, even after removal cell differentiation. mitigated effects, reducing acetylation promoting methylation. Conclusions: demonstrates potential modulating inflammation-induced preserving adipocyte function.

Язык: Английский

Процитировано

0