RESUMEN
This article aimed to investigate the role of miR-208 in the apoptosis of myocardial tissues in acute myocardial infarction (AMI) mice. The AMI mouse model was constructed. Then, miR-208 expression in AMI mice was regulated by transfection. The mouse myocardial tissues were subject to hematoxylin-eosin (HE) staining, TUNEL assay, and immunofluorescence analysis. H9c2 cell transfection and hypoxia induction were then completed, and cell apoptosis and cytokine levels were tested. Additionally, RNA pull-down and dual luciferase reporter gene assays were conducted for exploring the relation of miR-208 with programmed cell death 4 (PDCD4). Additionally, fluorescence in situ hybridization (FISH) was conducted for investigating miR-208 and PDCD4 colocalization within H9c2 cells. AMI mice had severe damage, apoptosis, decreased miR-208 expression, increased IL-1ß, IL-6, IL-8 levels, whereas reduced IL-10 level within myocardial tissues. H9c2 cells under hypoxia induction exhibited decreased miR-208 expression, promoted apoptosis, increased protein expression of Bax and cleaved-caspase-3, decreased protein expression of Bcl-2 and caspase-3, elevated IL-1ß, IL-6, IL-8 levels and decreased IL-10 level. miR-208 upregulation alleviated the damage and apoptosis of myocardial tissues in AMI mice. AMI mice with miR-208 upregulation showed decreased expression of Bax and cleaved-caspase-3, increased expression of Bcl-2 and caspase-3, reduced levels of IL-1ß, IL-6, IL-8, whereas an increased level of IL-10. miR-208 showed direct inhibition of PDCD4. PDCD4 and miR-208 were mainly co-expressed in the cytoplasm. The upregulated PDCD4 expression abolished miR-208's suppression of H9c2 cell apoptosis induced by hypoxia. Besides this, miR-208 inhibited myocardial tissue apoptosis in AMI mice by inhibiting PDCD4 expression.
Asunto(s)
Proteínas Reguladoras de la Apoptosis , MicroARNs , Infarto del Miocardio , Animales , Ratones , Apoptosis/genética , Proteínas Reguladoras de la Apoptosis/genética , Proteínas Reguladoras de la Apoptosis/metabolismo , Proteína X Asociada a bcl-2/metabolismo , Caspasa 3/metabolismo , Hipoxia/metabolismo , Hibridación Fluorescente in Situ , Interleucina-10/metabolismo , Interleucina-6/metabolismo , Interleucina-8/metabolismo , MicroARNs/metabolismo , Infarto del Miocardio/genética , Infarto del Miocardio/metabolismo , Miocitos Cardíacos/metabolismo , Proteínas Proto-Oncogénicas c-bcl-2/metabolismoRESUMEN
The utility of superb microvascular imaging (SMI) for evaluating hand joint lesions in patients with rheumatoid arthritis (RA) in clinical remission is unreported. This study aimed to compare SMI and power Doppler imaging (PDI) for the evaluation of hand joint lesions in these patients. Twenty-six patients with RA in clinical remission were enrolled. A total of 572 joints (52 wrist, 260 proximal interphalangeal, and 260 metacarpophalangeal joints) were detected by SMI and PDI. A semi-quantitative scale of 0-3 was used to compare the detection of synovial blood flow signal by SMI and PDI. Inter-observer agreement for the assessment of SMI and PDI scores was measured with kappa values. In the ten healthy volunteers, SMI and PDI signals were both scored 0. In the 26 RA patients, the remission rate via PDI was 65.4% but was only 42.3% via SMI. SMI also detected microvessel flow signal in seven patients diagnosed with clinical remission via PDI. Moreover, a total of 106 blood flow signals (18.5%) were detected by SMI, while 50 blood flow signals (8.7%) were detected by PDI. Compared with PDI, SMI increased 18.0% of power flow signals from Grade 0-1 and increased 13.7% of power flow signals from Grade 1-2. One joint classified as Grade 1 by PDI was classified as Grade 0 by SMI. Inter-observer agreement for PDI and SMI semi-quantitative scoring was moderate (kappa = 0.463). SMI seems more sensitive than PDI for detecting hand joint lesions in RA in clinical remission PDI, and could aid the achievement of true remission in RA patients.