دورية أكاديمية

miR-320c Regulates SERPINA1 Expression and Is Induced in Patients With Pulmonary Disease

التفاصيل البيبلوغرافية
العنوان: miR-320c Regulates SERPINA1 Expression and Is Induced in Patients With Pulmonary Disease
المؤلفون: Matamala, Nerea, Lara, Beatriz, Gomez-Mariano, Gema Maria, Martinez Rodríguez, Selene, Vázquez-Domínguez, Irene, Otero-Sobrino, Álvaro, Muñoz-Callejas, Antonio, Sánchez, Elena, Esquinas, Cristina, Bustamante, Ana, Cadenas, Sergio, Curi, Sergio, Lázaro, Lourdes, Martínez, María Teresa, Rodríguez, Esther, Miravitlles, Marc, Torres-Duran, María, Herrero, Inés, Michel, Francisco Javier, Castillo, Silvia, Hernández-Pérez, José Mª, Blanco, Ignacio, Casas, Francisco, Martinez-Delgado, Beatriz
المساهمون: Instituto de Salud Carlos III, Sociedad Española de Neumología y Cirugía Torácica
بيانات النشر: Sociedad Española de Patología Respiratoria
سنة النشر: 2021
المجموعة: REPISALUD (REPositorio Institucional en SALUD del Instituto de Salud Carlos III - ISCIII)
مصطلحات موضوعية: microRNA, miR-320c, Alpha-1 antitrypsin deficiency, Lung disease, Inflammation, Lung Diseases, MicroRNAs, alpha 1-Antitrypsin, alpha 1-Antitrypsin Deficiency, 3' Untranslated Regions, Humans, Lung
الوصف: Introduction: Alpha-1 antitrypsin deficiency (AATD) is a genetic condition resulting in lung and liver disease with a great clinical variability. MicroRNAs have been identified as disease modifiers; therefore miRNA deregulation could play an important role in disease heterogeneity. Members of miR-320 family are involved in regulating of multiple processes including inflammation, and have potential specific binding sites in the 3'UTR region of SERPINA1 gene. In this study we explore the involvement of miR-320c, a member of this family, in this disease. Methods: Firstly in vitro studies were carried out to demonstrate regulation of SERPINA1 gene by miR-320. Furthermore, the expression of miR-320c was analyzed in the blood of 98 individuals with different AAT serum levels by using quantitative PCR and expression was correlated to clinical parameters of the patients. Finally, HL60 cells were used to analyze induction of miR-320c in inflammatory conditions. Results: Overexpression of miR-320 members in human HepG2 cells led to inhibition of SERPINA1 expression. Analysis of miR-320c expression in patient's samples revealed significantly increased expression of miR-320c in individuals with pulmonary disease. Additionally, HL60 cells treated with the pro-inflammatory factor lipopolysaccharide (LPS) showed increase in miR-320c expression, suggesting that miR-320c responds to inflammation. Conclusion: Our findings demonstrate that miR-320c inhibits SERPINA1 expression in a hepatic cell line and its levels in blood are associated with lung disease in a cohort of patients with different AAT serum levels. These results suggest that miR-320c can play a role in AAT regulation and could be a biomarker of inflammatory processes in pulmonary diseases. ; This study was financed by grants from the Institute of Health Carlos III (AESI PI14CIII/00070 and PI17CIII/00042) and SEPAR (Sociedad Española de Neumología y Cirugía Torácica), project 92/2014. ; Sí
نوع الوثيقة: article in journal/newspaper
اللغة: English
تدمد: 1579-2129
العلاقة: https://doi.org/10.1016/j.arbr.2020.03.031Test; info:fis/Instituto de Salud Carlos III/null/null/ISCIII Subprograma de proyectos de investigacion en salud . Modalidad proyectos en salud. (2014)/PI14CIII/00070; info:fis/Instituto de Salud Carlos III/Programa Estatal de Fomento de la Investigación Científica y Técnica de Excelencia/Subprograma Estatal de Generación de Conocimiento/PI17-ISCIII Modalidad Proyectos de Investigacion en Salud Intramurales. (2017)/PI17CIII/00042; Arch Bronconeumol. 2021 Jul;57(7):457-463.; http://hdl.handle.net/20.500.12105/17267Test; Archivos de bronconeumologia
DOI: 10.1016/j.arbr.2020.03.031
الإتاحة: https://doi.org/20.500.12105/17267Test
https://doi.org/10.1016/j.arbr.2020.03.031Test
https://hdl.handle.net/20.500.12105/17267Test
حقوق: http://creativecommons.org/licenses/by-nc-nd/4.0Test/ ; Attribution-NonCommercial-NoDerivatives 4.0 Internacional ; open access
رقم الانضمام: edsbas.534A111B
قاعدة البيانات: BASE
الوصف
تدمد:15792129
DOI:10.1016/j.arbr.2020.03.031