Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12104/42233
Title: Inhibitors of MAPK pathway ERK1/2 or p38 prevent the IL-1?-induced up-regulation of SRP72 autoantigen in jurkat cells
Author: Stein, K.
Vasquez-Garibay, E.
Kratzsch, J.
Romero-Velarde, E.
Jahreis, G.
Issue Date: 2006
Abstract: Context: Leptin might be more important as a starvation hormone than as a satiety signal. The role of the soluble leptin receptor (sOB-R) and its regulation in children with protein energy malnutrition (PEM) is poorly understood. Design: We elucidated the effect of intensive nutritional support on the leptin axis in 26 severely malnourished toddlers who received infant milk-based formula for 2 wk via continuous enteral tube feeding followed by 2 wk ad libitum feeding. Serum levels of leptin, sOB-R, IGF-I, and IGF-binding protein-3 as well as anthropometric measurements were determined at the beginning of the study and at 2-wk intervals. The control group consisted of 13 well-nourished children. Results: The following were changes in the PEM toddlers after the nutritional support. Leptin increased significantly (P < 0.001), reaching 166% of levels observed in control group. sOB-R decreased significantly (P < 0.001), and a 142-fold molar excess of sOB-R over leptin was found. There were significant correlations between leptin and IGF-I after 2 wk and IGF-binding protein-3 during the whole study. sOB-R was not correlated with any anthropometric data, whereas IGF-I was a predictor of sOB-R variance in the PEM toddlers (19.9%, P = 0.022). Conclusion: It can be concluded that sOB-R has a modulatory effect on leptin in PEM children during nutritional recovery and participates in their adaptive survival mechanisms. Leptin and the molar excess of sOB-R over leptin are better biomarkers of nutritional status than IGF-I in PEM children during nutritional recovery. Copyright " 2006 by The Endocrine Society.",,,,,,"10.1210/jc.2005-1394",,,"http://hdl.handle.net/20.500.12104/42233","http://www.scopus.com/inward/record.url?eid=2-s2.0-33644823425&partnerID=40&md5=4939d16787ad5b2eab30d28e85fdebe3",,,,,,"3",,"Journal of Clinical Endocrinology and Metabolism",,"1021
1026",,"91",,"Scopus",,,,,,,,,,,,"Influence of nutritional recovery on the leptin axis in severely malnourished children",,"Article" "44042","123456789/35008",,"Arana-Argaez, V.E., Instituto de Investigacion en Reumatologia Y del Sistema Musculo Esqueletico, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco CP 44340, Mexico; Delgado-Rizo, V., Laboratorio de Inmunología, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco CP 44340, Mexico; Pizano-Martínez, O.E., Laboratorio de Inmunología, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco CP 44340, Mexico; Martínez-García, E.A., Instituto de Investigacion en Reumatologia Y del Sistema Musculo Esqueletico, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco CP 44340, Mexico; Martín-Márquez, B.T., Instituto de Investigacion en Reumatologia Y del Sistema Musculo Esqueletico, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco CP 44340, Mexico; Muñoz-Gómez, A., Instituto de Investigacion en Reumatologia Y del Sistema Musculo Esqueletico, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco CP 44340, Mexico, Pasante de Servicio Social en Medicina, Universidad Autónoma de Guadalajara, Guadalajara, Jalisco CP 45129, Mexico; Petri, M.H., Instituto de Investigacion en Reumatologia Y del Sistema Musculo Esqueletico, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco CP 44340, Mexico; Armendáriz-Borunda, J., Instituto de Biología Molecular en Medicina, Departamento de Biología Molecular Y Genómica, Universidad de Guadalajara, Guadalajara, Jalisco CP 44340, Mexico; Espinosa-Ramírez, G., Instituto de Investigacion en Reumatologia Y del Sistema Musculo Esqueletico, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco CP 44340, Mexico; Zúñiga-Tamayo, D.A., Instituto de Investigacion en Reumatologia Y del Sistema Musculo Esqueletico, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco CP 44340, Mexico; Herrera-Esparza, R., Universidad Autónoma de Zacatecas, Zacatecas, CP 98000, Mexico; Vázquez-Del Mercado, M., Instituto de Investigacion en Reumatologia Y del Sistema Musculo Esqueletico, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco CP 44340, Mexico, División de Medicina Interna, Departamento de Reumatología, Hospital Civil Dr. Juan I. Menchaca, Guadalajara, Jalisco CP 44340, Mexico",,"Arana-Argaez, V.E.
Delgado-Rizo, V.
Pizano-Martinez, O.E.
Martinez-García, E.A.
Martin-Marquez, B.T.
Munoz-Gomez, A.
Petri, M.H.
Armendariz-Borunda, J.
Espinosa-Ramirez, G.
Zuniga-Tamayo, D.A.
Herrera-Esparza, R.
Vazquez-Del Mercado, M.",,"2010",,"Phosphorylation is the most important post-translational event at a cellular level that is regulated by protein kinases. MAPKis a key player in the important cellular signaling pathway. It has been hypothesized that phosphorylation might have a role in the induction of break tolerance against some autoantigens such as SRP72. The aim of this study was to explore the pathways of phosphorylation and overexpression of the SRP72 polypeptide, using an in vitro model of Jurkat cells stimulated by recombinant human (rh)IL-1? in the presence of MAPK inhibitors. We used Jurkat cells as a substrate stimulated with rhIL-1? in the presence of MAPK inhibitors at different concentrations in a time course in vitro experiment by immunoprecipitation, immunoprecipitation-Western blotting, and real time PCR. Our results showed that rhIL-1? causes up-regulation of protein expression and phosphorylation of SRP72 in Jurkat cells. Inhibitors of the MAPK pathway ERK1/2 or p38?/? down-regulate the expression of SRP72 autoantigen in Jurkat cells stimulated by rhIL-1?. Our results highlight the importance of studying the pathways of activation and overexpression of autoantigens. It will be necessary to perform careful research on various kinases pathways, including MAPK in dermatomyositis and other rheumatic diseases, to help to explain the routes of activation and inhibition of autoantigens. The understanding of this process may help to develop new therapies to prevent and control the loss of tolerance toward own normal proteins. " 2010 by The American Society for Biochemistry and Molecular Biology, Inc.
URI: http://hdl.handle.net/20.500.12104/42263
http://www.scopus.com/inward/record.url?eid=2-s2.0-77958491259&partnerID=40&md5=4b0cb961632b3d2ff6d7c2639622964e
http://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&D=med5&AN=20729213
Appears in Collections:Producción científica UdeG

Files in This Item:
There are no files associated with this item.


Items in RIUdeG are protected by copyright, with all rights reserved, unless otherwise indicated.