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oai:repisalud.isciii.es:20.500.12105/172672025-05-09T09:22:42Zcom_20.500.12105_15322com_20.500.12105_2051com_20.500.12105_2052col_20.500.12105_16979col_20.500.12105_19616col_20.500.12105_16987

00925njm 22002777a 4500 dc Matamala, Nerea author Lara, Beatriz author Gomez-Mariano, Gema Maria author Martinez Rodríguez, Selene author Vazquez-Dominguez, Irene author Otero-Sobrino, Álvaro author Muñoz-Callejas, Antonio author Sánchez, Elena author Esquinas, Cristina author Bustamante, Ana author Cadenas, Sergio author Curi, Sergio author Lázaro, Lourdes author Martínez, María Teresa author Rodríguez, Esther author Miravitlles, Marc author Torres-Durán, María author Herrero, Inés author Michel, Francisco Javier author Castillo, Silvia author Hernández-Pérez, José Mª author Blanco, Ignacio author Casas, Francisco author Martinez-Delgado, Beatriz author 2021-07 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. Arch Bronconeumol. 2021 Jul;57(7):457-463. 10.1016/j.arbr.2020.03.031 1579-2129 Archivos de bronconeumologia 35698951 http://hdl.handle.net/20.500.12105/17267 microRNA miR-320c Alpha-1 antitrypsin deficiency Lung disease Inflammation miR-320c Regulates SERPINA1 Expression and Is Induced in Patients With Pulmonary Disease