Journal
INFLAMMATION RESEARCH
Volume 70, Issue 5, Pages 605-618Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00011-021-01462-1
Keywords
Adipokines; Glycine receptor; Inflammation; siRNA; TNF-α receptor
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Funding
- postdoctoral grant PRODEP (Programa para el Desarrollo Profesional Docente) de la Universidad Autonoma Metropolitana -Iztapalapa [UAM-I-CA-15]
- PRODEP-SEP
- Special Program Support to the Investigation, UAM-2019
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The study showed that glycine could partially inhibit the binding of TNF-alpha to its receptor, thereby inhibiting the secretion of pro-inflammatory adipokines in adipocytes through the TNF-alpha receptor mechanism.
Objective To determine the involvement of TNF-alpha 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-alpha and IL-6 mRNA were measured by qRT-PCR, while concentrations were quantified by ELISA. Results Glycine decreased the expression and concentration of TNF-alpha and IL-6; this effect did not occur in the absence of TNF-alpha receptor due to siRNA. In contrast, glycine produced only slight changes in the expression of TNF-alpha 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-alpha 1a receptor. Conclusion These findings support the idea that glycine could partially inhibit the binding of TNF-alpha to its receptor and provide clues about the mechanisms by which glycine inhibits the secretion of pro-inflammatory adipokines in adipocytes through the TNF-alpha receptor.
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