Rodrigo Romero-Nava1,2,3, Francisco J Alarcón-Aguilar1, Abraham Giacoman-Martínez1, Gerardo Blancas-Flores1, Karla A Aguayo-Cerón3, Martha A Ballinas-Verdugo4, Fausto Sánchez-Muñoz4, Fengyang Huang2, Santiago Villafaña-Rauda3, Julio C Almanza-Pérez5. 1. 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. 2. Departamento de Farmacología y Toxicología, Hospital Infantil de México Federico Gómez, Mexico City, Mexico. 3. Sección de Posgrado, Laboratorio de Señalización Intracelular, Escuela Superior de Medicina del Instituto Politécnico Nacional, Mexico City, Mexico. 4. Departamento de Inmunología, Instituto Nacional de Cardiología (Ignacio Chávez), Mexico City, Mexico. 5. 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. jcap@xanum.uam.mx.
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.
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.
Authors: Gerardo Blancas-Flores; Francisco J Alarcón-Aguilar; Rebeca García-Macedo; Julio C Almanza-Pérez; José L Flores-Sáenz; Rubén Román-Ramos; José L Ventura-Gallegos; Jesús Kumate; Alejandro Zentella-Dehesa; Miguel Cruz Journal: Eur J Pharmacol Date: 2012-06-23 Impact factor: 4.432
Authors: P H Carter; P A Scherle; J K Muckelbauer; M E Voss; R Q Liu; L A Thompson; A J Tebben; K A Solomon; Y C Lo; Z Li; P Strzemienski; G Yang; N Falahatpisheh; M Xu; Z Wu; N A Farrow; K Ramnarayan; J Wang; D Rideout; V Yalamoori; P Domaille; D J Underwood; J M Trzaskos; S M Friedman; R C Newton; C P Decicco; J A Muckelbauer Journal: Proc Natl Acad Sci U S A Date: 2001-10-09 Impact factor: 11.205
Authors: J C Almanza-Perez; F J Alarcon-Aguilar; G Blancas-Flores; A E Campos-Sepulveda; R Roman-Ramos; R Garcia-Macedo; M Cruz Journal: Biomed Pharmacother Date: 2009-10-17 Impact factor: 6.529