RESUMEN
BACKGROUND: Atherosclerosis (AS) is the most common type in cardiovascular disease. Due to its complex pathogenesis, the exact etiology of AS is unclear. circRNA has been shown to play an essential role in most diseases. However, the underlying mechanism of circRNA in AS has been not understood clearly. METHODS: Quantitative Real-Time PCR assay was used to detect the expression of circRSF1, miR-135b-5p and histone deacetylase 1 (HDAC1). Western blot was applied to the measure of protein expression of HDAC1, B-cell lymphoma-2 (Bcl-2), BCL2-associated X (Bax), cleaved-caspase-3, vascular cell adhesion molecule 1 (VCAM1), intercellular cell adhesion molecule-1 (ICAM1) and E-selectin. MTT assay and flow cytometry were used to detect cell proliferation and apoptosis, respectively. Dual luciferase reporter assay and RIP assay was used to determine the relationship among circRSF1, miR-135b-5p and HDAC1. Besides, an ELISA assay was performed to measure the levels of IL-1ß, IL-6, TNF-α and IL-8. RESULTS: In this study, ox-LDL inhibited circRSF1 and HDAC1 expression while upregulated miR-135b-5p expression in Human umbilical vein endothelial cells (HUVECs). Importantly, ox-LDL could inhibit HUVECs growth. Moreover, promotion of circRSF1 or inhibition of miR-135b-5p induced cell proliferation while inhibited apoptosis and inflammation of ox-LDL-treated HUVECs, which was reversed by upregulating miR-135b-5p or downregulating HDCA1 in ox-LDL-treated HUVECs. More than that, we verified that circRSF1 directly targeted miR-135b-5p and HDAC1 was a target mRNA of miR-135b-5p in HUVECs. CONCLUSION: CircRSF1 regulated ox-LDL-induced vascular endothelial cell proliferation, apoptosis and inflammation through modulating miR-135b-5p/HDAC1 axis in AS, providing new perspectives and methods for the treatment and diagnosis of AS.
Asunto(s)
Aterosclerosis , MicroARNs , Apoptosis/genética , Aterosclerosis/genética , Proliferación Celular , Histona Desacetilasa 1/genética , Células Endoteliales de la Vena Umbilical Humana , Humanos , Inflamación/genética , Lipoproteínas LDL , MicroARNs/genética , Proteínas Nucleares , ARN Circular , TransactivadoresRESUMEN
BACKGROUND: Atherosclerosis (AS) is the most common type in cardiovascular disease. Due to its complex pathogenesis, the exact etiology of AS is unclear. circRNA has been shown to play an essential role in most diseases. However, the underlying mechanism of circRNA in AS has been not understood clearly. METHODS: Quantitative Real-Time PCR assay was used to detect the expression of circRSF1, miR-135b-5p and histone deacetylase 1 (HDAC1). Western blot was applied to the measure of protein expression of HDAC1, B-cell lymphoma-2 (Bcl-2), BCL2-associated X (Bax), cleaved-caspase-3, vascular cell adhesion molecule 1 (VCAM1), intercellular cell adhesion molecule-1 (ICAM1) and E-selectin. MTT assay and flow cytometry were used to detect cell proliferation and apoptosis, respectively. Dual luciferase reporter assay and RIP assay was used to determine the relationship among circRSF1, miR-135b-5p and HDAC1. Besides, an ELISA assay was performed to measure the levels of IL-1ß, IL-6, TNF-α and IL-8. RESULTS: In this study, ox-LDL inhibited circRSF1 and HDAC1 expression while upregulated miR-135b-5p expression in Human umbilical vein endothelial cells (HUVECs). Importantly, ox-LDL could inhibit HUVECs growth. Moreover, promotion of circRSF1 or inhibition of miR-135b-5p induced cell proliferation while inhibited apoptosis and inflammation of ox-LDL-treated HUVECs, which was reversed by upregulating miR-135b-5p or downregulating HDCA1 in oxLDL-treated HUVECs. More than that, we verified that circRSF1 directly targeted miR-135b-5p and HDAC1 was a target mRNA of miR-135b-5p in HUVECs. CONCLUSION: CircRSF1 regulated ox-LDL-induced vascular endothelial cell proliferation, apoptosis and inflammation through modulating miR-135b-5p/HDAC1 axis in AS, providing new perspectives and methods for the treatment and diagnosis of AS.
Asunto(s)
Humanos , MicroARNs/genética , Aterosclerosis/genética , Proteínas Nucleares , Transactivadores , Apoptosis/genética , Proliferación Celular , Histona Desacetilasa 1/genética , Células Endoteliales de la Vena Umbilical Humana , ARN Circular , Inflamación/genética , Lipoproteínas LDLRESUMEN
Organophosphate esters (OPEs) were comprehensively investigated in the air samples collected using high-volume samplers near the Chinese Great Wall Station in the Western Antarctic Peninsula over the period of 2014-2018. The concentrations of ∑8OPEs (gaseous + particle phases) ranged from 33.9 to 404 pg/m3 with a geometric mean of 119 ± 12.0 pg/m3. Tris [(2R)-1-chloro-2-propyl] phosphate (TCIPP) and tris(2-chloroethyl) phosphate (TCEP) dominated in the gaseous phase, while tris-n-butyl phosphate (TnBP) was the most abundant OPEs in the particle phase, followed by TCIPP and TCEP. An apparently temporal trend was observed for atmospheric ∑8OPEs over the five years, with a doubling time of about 3.8 years, which indicated continuous inputs of OPEs into the sampling area. The particle-bound ∑8OPEs accounted for 45% of the total, generally lower than that reported in the Arctic. Gas-particle partitioning modeling suggested that the partitioning of OPEs with higher logKOA values approached the steady state in the Antarctic air. The back-trajectory modeling showed that high levels of OPEs were usually associated with air inputs from the northwest of the peninsula. This suggested that long-range transport from South America, which was confirmed by the no temperature dependencies of OPEs concentrations (excluding TnBP). Nevertheless, a steady high level of particle-bound TnBP implied local sources in the Western Antarctic Peninsula, which required further investigation in future works.
Asunto(s)
Ésteres , Retardadores de Llama , Regiones Antárticas , Regiones Árticas , China , Monitoreo del Ambiente , Retardadores de Llama/análisis , Organofosfatos , América del SurRESUMEN
OBJECTS: The retrospective study aimed to determine the prevalence rate and antimicrobial susceptibility of extended-spectrum beta-lactamases (ESBLs)-producing Klebsiella pneumoniae and Escherichia coli in 2013-2017 at a single center in China. METHODS: Klebsiella pneumoniae and Escherichia coli data were collected from the microbiological laboratory. VITEK 2 compact system was used for the identification and antimicrobial susceptibility testing. ESBL status was determined as per the Clinical and Laboratory Standards Institute (CLSI) protocols microdilution method. RESULTS: Among a total of 2774 strains of Klebsiella pneumoniae and 2154 strains of Escherichia coli, 15.79% and 36.86% were found to be ESBL producers, respectively. In all patients infected by ESBLs-producing strains, those over 60 years accounted for the largest proportion. Infection by ESBLs-producing Klebsiella pneumoniae was more common in male, while that by ESBLs-producing Escherichia coli was more common in female. Urine and respiratory secretions were the most common sources of ESBLs-producing strains; however, ESBLs-producing strains from urine had been significantly declined. No carbapenem-resistant isolate was found, and all ESBLs-producing strains were resistant to ceftriaxone, aztreonam, and piperacillin. There were no differences in resistance rates between ESBLs-producing Escherichia coli and Klebsiella pneumoniae to ceftazidime and cefepime; however, ESBLs-producing Klebsiella pneumoniae showed higher resistance rates to piperacillin/tazobactam, amikacin, gentamicin, and co-trimoxazole compared with ESBLs-producing Escherichia coli. CONCLUSION: Different ESBLs-producing organisms have their own epidemiological characteristics, and the resistance of ESBLs-producing Klebsiella pneumoniae and Escherichia coli is different even to the same antibiotics. Therefore, it is important to continuously monitor the status of ESBLs-producing organisms, and an improved antimicrobial stewardship and infection control are much required.