Glycine is a competitive antagonist of the TNF receptor mediating the expression of inflammatory cytokines in 3T3-L1 adipocytes

Objective To determine the involvement of TNF-α and glycine receptors in the inhibition of pro-inflammatory adipokines in 3T3-L1 cells. Methods RT-PCR evidenced glycine receptors in 3T3-L1 adipocytes. 3T3-L1 cells were transfected with siRNA for the glycine (Glrb) and TNF1a (Tnfrsf1a) receptors and...

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Published inInflammation research Vol. 70; no. 5; pp. 605 - 618
Main Authors Romero-Nava, Rodrigo, Alarcón-Aguilar, Francisco J., Giacoman-Martínez, Abraham, Blancas-Flores, Gerardo, Aguayo-Cerón, Karla A., Ballinas-Verdugo, Martha A., Sánchez-Muñoz, Fausto, Huang, Fengyang, Villafaña-Rauda, Santiago, Almanza-Pérez, Julio C.
Format Journal Article
LanguageEnglish
Published Cham Springer International Publishing 01.05.2021
Springer Nature B.V
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Summary:Objective To determine the involvement of TNF-α and glycine receptors in the inhibition of pro-inflammatory adipokines in 3T3-L1 cells. Methods RT-PCR evidenced glycine receptors in 3T3-L1 adipocytes. 3T3-L1 cells were transfected with siRNA for the glycine (Glrb) and TNF1a (Tnfrsf1a) receptors and confirmed by confocal microscopy. Transfected cells were treated with glycine (10 mM). The expressions of TNF-α and IL-6 mRNA were measured by qRT-PCR, while concentrations were quantified by ELISA. Results Glycine decreased the expression and concentration of TNF-α and IL-6; this effect did not occur in the absence of TNF-α receptor due to siRNA. In contrast, glycine produced only slight changes in the expression of TNF-α and IL-6 in the absence of the glycine receptor due to siRNA. A docking analysis confirmed the possibility of binding glycine to the TNF-α1a receptor. Conclusion These findings support the idea that glycine could partially inhibit the binding of TNF-α to its receptor and provide clues about the mechanisms by which glycine inhibits the secretion of pro-inflammatory adipokines in adipocytes through the TNF-α receptor.
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ISSN:1023-3830
1420-908X
DOI:10.1007/s00011-021-01462-1