RESUMO
Atherosclerosis (AS) is a chronic inflammatory vascular disease that begins with endothelial activation followed by a series of inflammatory responses, plaque formation, and finally rupture. An early event in endothelial dysfunction is activation of the nuclear factor-κB (NF-κB) signaling axis. Toll-like receptors (TLRs) in endothelial cells (ECs) play an essential role in recognizing pathogen-associated molecular patterns (PAMPs), damage-associated molecular patterns (DAMPs), and lifestyle-associated molecular patterns (LAMPs). Activation of the canonical NF-κB pathway stimulates the expression of cytokines, chemokines, and an array of additional genes which activate and amplify AS-associated inflammatory responses. In this review, we discuss the involvement of TLR2/4 and NF-κB signaling in ECs during AS initiation, as well as regulation of the inflammatory response during AS by noncoding RNAs, especially microRNA (miRNA) and circular RNA (circRNA).
Assuntos
Aterosclerose , Células Endoteliais , NF-kappa B , Transdução de Sinais , Receptor 2 Toll-Like , Receptor 4 Toll-Like , Humanos , Aterosclerose/metabolismo , Aterosclerose/imunologia , NF-kappa B/metabolismo , Células Endoteliais/metabolismo , Receptor 2 Toll-Like/metabolismo , Receptor 2 Toll-Like/genética , Receptor 4 Toll-Like/metabolismo , Receptor 4 Toll-Like/genética , MicroRNAs/genética , MicroRNAs/metabolismo , Animais , RNA Circular/genética , RNA Circular/metabolismo , RNA Circular/fisiologia , Inflamação/metabolismoRESUMO
Atherosclerosis is a lipid-driven inflammatory arterial disease, with one crucial factor is oxidized low-density lipoprotein (ox-LDL), which can induce endothelial dysfunction through endoplasmic reticulum stress (ERS). Interleukin-37 (IL-37) exerts vascular protective functions. This study aims to investigates whether IL-37 can alleviate ERS and autophagy induced by ox-LDL, therely potentialy treating atherosclerosis. We found that ox-LDL enhances the wound healing rate in Rat Coronary Artery Endothelial Cells (RCAECs) and IL-37 reduce the ox-LDL-induced pro-osteogenic response, ERS, and autophagy by binding to Smad3. In RCAECs treated with ox-LDL and recombinant human IL-37, the wound healing rate was mitigated. The expression of osteogenic transcription factors and proteins involved in the ERS pathway was reduced in the group pretreated with IL-37 and ox-LDL. However, these responses were not alleviated when Smads silenced. Electron microscopy revealed that the IL-37/Smad3 complex could suppress endoplasmic reticulum autophagy under ox-LDL stimulation. Thus, IL-37 might treat atherosclerosis through its multi-protective effect by binding Smad3.
Assuntos
Aterosclerose , Células Endoteliais , Interleucina-1 , Animais , Humanos , Ratos , Aterosclerose/tratamento farmacológico , Aterosclerose/prevenção & controle , Aterosclerose/metabolismo , Lipoproteínas LDL/farmacologia , Lipoproteínas LDL/metabolismo , Fatores de Transcrição/metabolismo , Interleucina-1/uso terapêuticoRESUMO
In this work, a quartz crystal microbalance (QCM) sensor has been fabricated using immunoassay for sensitive determination of Bifidobacterium bifidum. Au nanoparticle has been used for amplifying sandwich assays. The proposed immunosensor exhibited a linear detection range between 103 and 105 CFU/mL with a limit of detection of 2.1 × 102 CFU/mL. The proposed immunosensor exhibited good selectivity for B. bifidum sensing with low cross reactivity for other foodborne pathogens such as Lactobacillus acidophilus, Listeria monocytogenes, and Escherichia coli. In addition, the proposed immunosensor has been successfully used for B. bifidum detection in feces samples and food samples. The frequency decreases of 12, 17, and 10 Hz were observed from the milk samples consisting of the mixtures of L. acidophilus, L. monocytogenes, and E. coli. The frequency decreases of 8, 15, and 7 Hz were observed from the feces samples consisting of the mixtures of L. acidophilus, L. monocytogenes, and E. coli.