KLF7 promotes adipocyte inflammation and glucose metabolism disorder by activating the PKCζ/NF-κB pathway.


Journal

FASEB journal : official publication of the Federation of American Societies for Experimental Biology
ISSN: 1530-6860
Titre abrégé: FASEB J
Pays: United States
ID NLM: 8804484

Informations de publication

Date de publication:
07 2023
Historique:
revised: 21 05 2023
received: 02 01 2023
accepted: 02 06 2023
medline: 23 6 2023
pubmed: 21 6 2023
entrez: 21 6 2023
Statut: ppublish

Résumé

In the obesity context, inflammatory cytokines secreted by adipocytes lead to insulin resistance and are key to metabolic syndrome development. In our previous study, we found that the transcription factor KLF7 promoted the expression of p-p65 and IL-6 in adipocytes. However, the specific molecular mechanism remained unclear. In the present study, we found that the expression of KLF7, PKCζ, p-IκB, p-p65, and IL-6 in epididymal white adipose tissue (Epi WAT) in mice fed a high-fat diet (HFD) was significantly increased. In contrast, the expression of PKCζ, p-IκB, p-p65, and IL-6 was significantly decreased in Epi WAT of KLF7 fat conditional knockout mice. In 3T3-L1 adipocytes, KLF7 promoted the expression of IL-6 via the PKCζ/NF-κB pathway. In addition, we performed luciferase reporter and chromatin immunoprecipitation assays, which confirmed that KLF7 upregulated the expression of PKCζ transcripts in HEK-293T cells. Collectively, our results show that KLF7 promotes the expression of IL-6 by upregulating PKCζ expression and activating the NF-κB signaling pathway in adipocytes.

Identifiants

pubmed: 37342904
doi: 10.1096/fj.202300005R
doi:

Substances chimiques

I-kappa B Proteins 0
Interleukin-6 0
NF-kappa B 0
protein kinase C zeta EC 2.7.11.1
Klf7 protein, mouse 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e23033

Informations de copyright

© 2023 The Authors. The FASEB Journal published by Wiley Periodicals LLC on behalf of Federation of American Societies for Experimental Biology.

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Auteurs

Xin Yang (X)

Department of Medical Genetics, Medical College of Shihezi University, Shihezi, China.

Maodi Liang (M)

Department of Medical Genetics, Medical College of Shihezi University, Shihezi, China.

Yihan Tang (Y)

Department of Medical Genetics, Medical College of Shihezi University, Shihezi, China.

Dingling Ma (D)

Department of Medical Genetics, Medical College of Shihezi University, Shihezi, China.

Menghuan Li (M)

Department of Medical Genetics, Medical College of Shihezi University, Shihezi, China.

Chenggang Yuan (C)

Department of Medical Genetics, Medical College of Shihezi University, Shihezi, China.

Yanting Hou (Y)

Department of Medical Genetics, Medical College of Shihezi University, Shihezi, China.

Chaoyue Sun (C)

Department of Medical Genetics, Medical College of Shihezi University, Shihezi, China.

Jie Liu (J)

Department of Medical Genetics, Medical College of Shihezi University, Shihezi, China.

Qianqian Wei (Q)

Department of Medical Genetics, Medical College of Shihezi University, Shihezi, China.

Yongsheng Chang (Y)

Department of Medical Genetics, Medical College of Shihezi University, Shihezi, China.
Department of Physiology and Pathophysiology, Tianjin Medical University, Tianjin, China.

Cuizhe Wang (C)

Department of Medical Genetics, Medical College of Shihezi University, Shihezi, China.

Jun Zhang (J)

Department of Medical Genetics, Medical College of Shihezi University, Shihezi, China.

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