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

Inflamm Res

Laboratorio de Farmacología, Departamento de Ciencias de la Salud, DCBS, Universidad Autónoma Metropolitana-Iztapalapa (UAM-I), San Rafael Atlixco 186, Col. Vicentina. Iztapalapa, C.P. 09340, Mexico City, Mexico.

Published: May 2021

AI Article Synopsis

  • The study investigates how glycine and TNF-α receptors affect the release of pro-inflammatory proteins in 3T3-L1 fat cells.
  • Glycine receptors were identified in these cells, and experiments showed that glycine can reduce levels of TNF-α and IL-6, but this effect depends on the presence of the TNF-α receptor.
  • The results suggest that glycine might reduce inflammation by interfering with TNF-α signaling, highlighting its potential role in regulating inflammatory responses in fat cells.

Article Abstract

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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Source
http://dx.doi.org/10.1007/s00011-021-01462-1DOI Listing

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