| Autor: |
Ashley A. Able, Allison J. Richard, Jacqueline M. Stephens |
| Jazyk: |
angličtina |
| Rok vydání: |
2023 |
| Předmět: |
|
| Zdroj: |
Biology, Vol 12, Iss 5, p 674 (2023) |
| Druh dokumentu: |
article |
| ISSN: |
2079-7737 |
| DOI: |
10.3390/biology12050674 |
| Popis: |
Impaired adipocyte function contributes to systemic metabolic dysregulation, and altered fat mass or function increases the risk of Type 2 diabetes. EHMTs 1 and 2 (euchromatic histone lysine methyltransferases 1 and 2), also known as the G9a-like protein (GLP) and G9a, respectively, catalyze the mono- and di-methylation of histone 3 lysine 9 (H3K9) and also methylate nonhistone substrates; in addition, they can act as transcriptional coactivators independent of their methyltransferase activity. These enzymes are known to contribute to adipocyte development and function, and in vivo data indicate a role for G9a and GLP in metabolic disease states; however, the mechanisms involved in the cell-autonomous functions of G9a and GLP in adipocytes are largely unknown. Tumor necrosis factor alpha (TNFα) is a proinflammatory cytokine typically induced in adipose tissue in conditions of insulin resistance and Type 2 diabetes. Using an siRNA approach, we have determined that the loss of G9a and GLP enhances TNFα-induced lipolysis and inflammatory gene expression in adipocytes. Furthermore, we show that G9a and GLP are present in a protein complex with nuclear factor kappa B (NF-κB) in TNFα-treated adipocytes. These novel observations provide mechanistic insights into the association between adipocyte G9a and GLP expression and systemic metabolic health. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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