Please use this identifier to cite or link to this item: https://repositorio.uca.edu.ar/handle/123456789/8618
Título : CFTR impairment upregulates c-Src activity through IL-1β autocrine signaling
Autor : Massip Copiz, María Macarena 
Clauzure, Mariángeles 
Valdivieso, Ángel Gabriel 
Santa Coloma, Tomás Antonio 
Palabras clave : FIBROSIS QUISTICAMITOCONDRIASGENES
Fecha de publicación : 2017
Editorial : Elsevier
Cita : Massip-Copiz MM, Clauzure M, Valdivieso ÁG, Santa-Coloma TA. CFTR impairment upregulates c-Src activity through IL-1β autocrine signaling [en línea]. Archives of Biochemistry and Biophysics. 2017;616:1-12. doi:10.1016/j.abb.2017.01.003 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8618
Resumen : Abstract: Cystic Fibrosis (CF) is a disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Previously, we found several genes showing a differential expression in CFDE cells (epithelial cells derived from a CF patient). One corresponded to c-Src; its expression and activity was found increased in CFDE cells, acting as a signaling molecule between the CFTR activity and MUC1 overexpression. Here we report that bronchial IB3-1 cells (CF cells) also showed increased c-Src activity compared to 'CFTR-corrected' S9 cells. In addition, three different Caco-2 cell lines, each stably transfected with a different CFTR-specific shRNAs, displayed increased c-Src activity. The IL-1β receptor antagonist IL1RN reduced the c-Src activity of Caco-2/pRS26 cells (expressing a CFTR-specific shRNA). In addition, increased mitochondrial and cellular ROS levels were detected in Caco-2/pRS26 cells. ROS levels were partially reduced by incubation with PP2 (c-Src inhibitor) or IL1RN, and further reduced by using the NOX1/4 inhibitor GKT137831. Thus, IL-1β→c-Src and IL-1β→NOX signaling pathways appear to be responsible for the production of cellular and mitochondrial ROS in CFTR-KD cells. In conclusion, IL-1β constitutes a new step in the CFTR signaling pathway, located upstream of c-Src, which is stimulated in cells with impaired CFTR activity.
URI : https://repositorio.uca.edu.ar/handle/123456789/8618
ISSN : 0003-9861
Disciplina: MEDICINA
DOI: 10.1016/j.abb.2017.01.003
Derechos: Acceso Abierto. 12 meses de embargo
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