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1.
Genet Mol Res ; 15(1)2016 Feb 05.
Artículo en Inglés | MEDLINE | ID: mdl-26909955

RESUMEN

This study investigated the effects induced by co-culturing human primary basic fibroblasts (HPBFs) with 16-human bronchial epithelial cells (16-HBE) infected with respiratory syncytial virus (RSV), in particular the transformation of HPBFs into myofibroblasts and secretion of extracellular matrix proteins. HPBFs were co-cultured with 16-HBE cells infected with RSV and quantitatively analyzed. We constructed models of HPBFs co-cultured with 16-HBE cells that were either uninfected (control group) or infected with RSV (experimental group). Following initiation of co-cultures, HPBFs and supernatants were collected at 24-h intervals up to 120 h. Expression of α-smooth muscle actin (α-SMA) was detected by indirect immunofluorescence and western blotting, while type I collagen (Col I) and fibronectin were analyzed by competitive enzyme-linked immunosorbent assays. After 72 h, α-SMA expression increased in HPBFs cultured with RSV-infected 16-HBE relative to uninfected controls, reaching its highest level at 96 h. Similarly, Col I secretion was also higher in HPBFs co-cultured with RSV-infected 16-HBE relative to uninfected controls; Col I secretion increased with time and reached its highest level at 120 h. HPBFs were transformed into myofibroblasts following co-culture with RSV-infected 16-HBE, which when combined with the observed increase in Col I secretion suggests that airway remodeling would then be promoted.


Asunto(s)
Remodelación de las Vías Aéreas (Respiratorias) , Células Epiteliales/virología , Fibroblastos/patología , Miofibroblastos/patología , Infecciones por Virus Sincitial Respiratorio/patología , Infecciones del Sistema Respiratorio/patología , Actinas/metabolismo , Bronquios/patología , Bronquios/virología , Técnicas de Cocultivo , Colágeno Tipo I/metabolismo , Células Epiteliales/patología , Fibroblastos/metabolismo , Fibronectinas/metabolismo , Humanos , Miofibroblastos/metabolismo , Infecciones por Virus Sincitial Respiratorio/metabolismo , Infecciones por Virus Sincitial Respiratorio/virología , Virus Sincitiales Respiratorios , Infecciones del Sistema Respiratorio/metabolismo , Infecciones del Sistema Respiratorio/virología
2.
Genet Mol Res ; 13(4): 8385-95, 2014 Oct 20.
Artículo en Inglés | MEDLINE | ID: mdl-25366732

RESUMEN

We explored the interaction of 6 candidate genetic mutations in essential hypertension (EH). The mutations AGT M235T, ACE I/D, eNOS Glu298Asp, ET-2 A985G, ANP T2238C, and NPRC A-55C were detected using a genechip microarray in 100 patients with EH and 97 controls from the Han population living in the Yunnan Province of China. Risks of EH were evaluated with respect to a combination of these genotypes. Interactions were analyzed using multifactor dimensionality reduction (MDR). P values were corrected using Bonferroni's adjustment. Results showed that CC genotype frequencies for NPRC A-55C (0.540) in EH were significantly higher than those in controls (0.237, Pc < 0.01; odds ratio (OR) = 3.777; 95% confidence interval (CI) = 2.050-6.960). The OR for NPRC A-55C CC combined with ET-2 A985G GG increased to 4.673 and to 5.529 when the MT genotype of AGT M235T, the EE genotype of eNOS Glu298Asp, the GG genotype of ET-2 A985G, and the CC genotype of NPRC A-55C were combined. MDR showed that ET-2/NPRC is the best model (OR = 4.002; 95%CI = 2.1597-7.4159). The CC genotype for NPRC A-55C and the G allele for ET-2 A985G were associated with susceptibility to EH. Although the contributions of the candidate genes differ, they may have cooperative effects on conferring risk for EH. Moreover, potential gene-gene interactions were found between ET-2 A985G and NPRC A-55C in EH.


Asunto(s)
Epistasis Genética , Hipertensión/genética , Anciano , Alelos , Estudios de Casos y Controles , Hipertensión Esencial , Femenino , Frecuencia de los Genes , Estudios de Asociación Genética , Sitios Genéticos , Genotipo , Humanos , Hipertensión/fisiopatología , Masculino , Persona de Mediana Edad , Oportunidad Relativa , Polimorfismo Genético
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