Upregulation of miR-223 by SIRT1 attenuates the inflammatory response in neonatal sepsis.

To investigate the effect of minocycline hydrochloride(MH) loaded nano-silica microspheres(MSNion) on the inflammatory regulation of periodontitis in rats. Mesoporous silica(MSN) was prepared by classical St?ber method and MSNion was obtained by doping hydroxyapatite. MH was loaded into MSNion by magnetic stirring, and chitosan (COS), which had anti-inflammatory and antibacterial effect, was adsorbed on its surface by using charge interactions, forming MH@MSNion@COS microspheres. The microspheres were characterized by electron microscopy and X-ray diffraction. The experiments were divided into control, MH, MSNion@COS and MH@MSNion@COS groups. The cytotoxicity of each group was assessed using the CCK-8 cell assay and the optimal concentration was determined. The expression levels of inflammatory factors(TNF-α, IL-6, IL-1β, iNOS, IL-10) were determined in each group using ELISA kits. In periodontitis model, the rats were treated according to the grouping of cell experiments, periodontal probing depth (PD) and gingival index (GI) of the rats were measured at 0, 1, 2, 4 weeks. At 4 weeks of the experiment, the peripheral blood of each group of rats was collected, and the levels of inflammatory factors in serum were detected by ELISA kits. Nanoparticles with a particle size of about 110 nm were prepared and observed as regular spheres by electron microscopy. MH@MSNion@COS degraded into fragments with unclear structure at the 8th day. In vitro drug release assay showed a slow release of MH, and the MH release rate reached 80% at about the 15th day. In cell experiment, MH@MSNion@COS showed the best cell proliferation activity at 50 μg/mL (P＜0.05), and the cell activity was higher than that of MH group and MSNion@COS group(P＜0.05). There was no significant difference between MH group and MSNion@COS group. ELISA results showed that the expression of inflammatory factors in MH@MSNion@COS group was significantly lower than that in LPS group at the first day(P＜0.01), and there was no significant difference between MH group and MSNion@COS group. At the 3rd day, the expression of M1 inflammatory factors in MH@MSNion@COS group was lower than that in control group, and the expression of M2 inflammatory factors was higher than that in control group(P＜0.05). PD and GI of MH@MSNion@COS group were significantly decreased after administration compared with other groups(P＜0.05), and the amount of inflammatory factors was lower than other groups(P＜0.05). MH@MSNion@COS has a good inflammatory regulation effect on experimental periodontitis in vitro and in vivo.

Objectives:To explore levels of anti-oxidative molecules and inflammatory factors in patients with vascular dementia (VD) and their clinical significance.Methods:Sixty VD patients admitted in our hospital from January 2016 to January 2019 were classified into an experimental group, while another 60 healthy patients seeking physical examinations in the corresponding period were selected as a control group. Various indexes related to serum inflammatory factors and anti-oxidative molecules were compared among patients in such two groups. For the purpose of comparing anti-oxidative molecular expression levels and inflammatory factor levels in patients with VD of different severities, 60 cases in the experimental group were divided, based on a Mini-mental State Examination (MMSE) scale, into patients with mild symptoms (n=20, score: 21~26), patients with moderate symptoms (n=22, score: 10~20) and patients with severe symptoms (n=18, score: 0~9).Results:By contrast to the control group, levels of inflammatory factors (e.g., TNF-a, CRP and IL-6) in VD patients are all significantly increased and their differences show statistical significance (p<0.05); and, expression levels of anti-oxidative factors, including superoxide dismutase (SOD), glutathion peroxidase (GSH-Px), total antioxidant capacity (TAC), catalase (CAT) and glutathione reductase (GR), in the experimental group are apparently below those of the control group (P<0.05). As dementia degree increases, expression levels of serum anti-oxidative molecules in such patients are inclined to drop in a significant way (P<0.05), while inflammatory factor levels tend to go up gradually (P<0.05).Conclusions:If compared with the normal population, inflammatory factor levels in serum of VD patients are higher; however, expression levels of anti-oxidative molecules become below those of the normal population. Additionally, levels of inflammatory factors and anti-oxidative molecules may change obviously as severity of illness increases. This suggests that inflammation and oxidation play a certain role of auxoaction in VD patients.

BackgroundHypothermia is associated with many adverse clinical outcomes in pediatric patients, and thus, it is important to find an effective and safe method for preventing peri-operative hypothermia and its associated adverse outcomes in pediatric patients. This study aimed to investigate the effect of forced-air warming blankets with different temperatures on changes in the transforming growth factor-β (TGF-β), tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-10 levels in children undergoing surgical treatment for developmental displacement of the hip (DDH).MethodsThe study included 123 children undergoing surgery for DDH under general anesthesia. The patients were randomly assigned to three groups, using a random number table: the 32, 38, and 43°C groups according to the temperature setting of the forced-air warming blankets. For each patient, body temperature was recorded immediately after anesthesia induction and intubation (T0), at initial incision (T1), at 1 h after incision (T2), at 2 h after incision (T3), at the end of surgery (T4), immediately upon return to the ward after surgery (T5), and then at 12 h (T6), 24 h (T7), 36 h (T8), and 48 h (T9) after the surgery. The serum levels of TGF-β, TNF-α, IL-1β, and IL-10 were measured at T0 and T4 for all groups.ResultsThe number of patients with fever in the 38°C group was significantly less than those in the 32 and 43°C groups (χ2 = 6.630, P = 0.036). At T0, the body temperatures in the 38 and 43°C groups were significantly higher than that in the 32°C group (F = 17.992, P < 0.001). At T2, the body temperature was significantly higher in the 43°C group than those in the 32 and 38°C groups (F = 12.776, P < 0.001). Moreover, at T4, the serum levels of TGF-β (F = 3286.548, P < 0.001) and IL-10 (F = 4628.983, P < 0.001) were significantly increased in the 38°C group, and the serum levels of TNF-α (F = 911.415, P < 0.001) and IL-1β (F = 322.191, P < 0.001) were significantly decreased in the 38°C group, compared with the levels in the 32 and 43°C groups.ConclusionForce-air warming blankets set at 38°C maintained stable body temperature with less adverse outcome and effectively inhibited the inflammatory response in pediatric patients undergoing surgery for DDH.Clinical trial registrationChiCTR1800014820; http://www.chictr.org.cn/showproj.aspx?proj=25240.

Activation of Kupffer cells (KCs) by gut-derived lipopolysaccharide (LPS) and Toll-Like Receptors 4 (TLR4)-LPS-mediated increase in TNFα production has a central role in the pathogenesis of alcoholic liver disease. Micro-RNA (miR)-125b, miR-146a, and miR-155 can regulate inflammatory responses to LPS. Here we evaluated the involvement of miRs in alcohol-induced macrophage activation. Chronic alcohol treatment in vitro resulted in a time-dependent increase in miR-155 but not miR-125b or miR-146a levels in RAW 264.7 macrophages. Furthermore, alcohol pretreatment augmented LPS-induced miR-155 expression in macrophages. We found a linear correlation between alcohol-induced increase in miR-155 and TNFα induction. In a mouse model of alcoholic liver disease, we found a significant increase in both miR-155 levels and TNFα production in isolated KCs when compared with pair-fed controls. The mechanistic role of miR-155 in TNFα regulation was indicated by decreased TNFα levels in alcohol-treated macrophages after inhibition of miR-155 and by increased TNFα production after miR-155 overexpression, respectively. We found that miR-155 affected TNFα mRNA stability because miR-155 inhibition decreased whereas miR-155 overexpression increased TNFα mRNA half-life. Using the NF-κB inhibitors, MG-132 or Bay11-7082, we demonstrated that NF-κB activation mediated the up-regulation of miR-155 by alcohol in KCs. In conclusion, our novel data demonstrate that chronic alcohol consumption increases miR-155 in macrophages via NF-κB and the increased miR-155 contributes to alcohol-induced elevation in TNFα production via increased mRNA stability.

The overexpression of SIRT1 inhibited osteoarthritic gene expression changes induced by interleukin‐1β in human chondrocytes

BackgroundCigarette smoking is a recognised environmental risk factor not only for the development of rheumatoid arthritis (RA), but also for the severity of established RA. Specifically, smoking is associated with...

To investigate the role of micro ribonucleic acid (miR)-181 in the inflammatory responses of osteoarthritis (OA) and related mechanism. The rat model of OA was established by anterior cruciate ligament (ACL) transection, and an automatic immuno-analyzer was applied to detect the bone metabolism indexes in the serum. The levels of relevant inflammatory factors in the joint fluid and serum were measured using enzyme-linked immunosorbent assay (ELISA). The cartilage specimens were collected to determine the expression of miR-181 in OA and normal cartilage tissues. Meanwhile, isolated cartilage cells were cultured and transfected with miR-181 mimics and inhibitor separately, and a blank control group was also included. Quantitative Real-time polymerase chain reaction (qRT-PCR) was adopted to detect the messenger RNA (mRNA) expressions of inflammatory factors [tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6)] in the cartilage cells. The expression levels of NF-κB and matrix metalloproteinase-13 (MMP-13) proteins related to the NF-κB signaling pathway were determined via Western blotting. In OA model group, the content of serum osteocalcin (OSTEOC) and vitamin D (VD) declined markedly (p<0.05), the content of parathyroid hormone (PTH) increased notably (p<0.05), whereas the change of β-Cross Laps was not significant. ELISA results showed that the levels of TNF-α, IL-6 and MMP-9 were elevated remarkably in OA model group (p<0.05). Compared with that in normal cartilage tissues, miR-181 expression was increased evidently in OA cartilage tissues (p<0.05). Moreover, miR-181 expression was also significantly elevated in miR-181 mimics group after transfection (p<0.05). The expressions of inflammatory factors TNF-α and IL-6 in the cartilage cells were increased remarkably in miR-181 mimics group compared with those in control group (p<0.05). The miR-181 inhibitor could significantly lower the expressions of inflammatory factors TNF-α and IL-6 (p<0.05). According to the results of Western blotting, the protein expressions of MMP-13 and NF-κB were decreased notably in miR-181 inhibitor group (p<0.05), but were evidently up-regulated in miR-181 mimics group (p<0.05). The decrease of miR-181 can reduce the expressions of inflammatory factors TNF-α and IL-6 through downregulating the NF-κB signaling pathway, thus repressing the occurrence of OA.

Silent mating type information regulation 2 homolog1 (SIRT1) is a multifaceted, nicotinamide adenine dinucleotide-dependent protein deacetylase with involvement in a wide variety of cellular processes ranging from cancer to aging. Expression of SIRT1 was evaluated in 90 cases of hepatocellular carcinoma (HCC) and five HCC cell lines. The relationship between the mutation status of p53 and expression of SIRT1 was also investigated in 10 fresh HCC tissues. Synthetic small interfering RNA was used to silence SIRT1 gene expression by RNA interference (RNAi), and cell growth and cell cycle progression were assessed. Expression of SIRT1 was significantly elevated in the HCC tissues when compared to that of non-tumor tissues (p<0.001). Overexpression of SIRT1 and p53 was observed in 56% (50 of 90) and in 30% (27 of 90) of the HCCs, respectively. Expression of SIRT1 showed significant correlation with gender (p=0.023), serum AFP levels (p=0.030), viral infection (p=0.005) and p53 expression (p<0.021). Western blot analysis found no correlation between p53 mutation and expression levels of SIRT1. SIRT1 silencing was found to induce cell growth arrest in HCC cells. These results suggest an association of SIRT1 expression with HCC development and that SIRT1 plays a role in cancer cell growth.

To investigate the expression of microRNA-29 a(miR-29 a) in the human steatotic hepatocyte model and the mechanism of targeting silent mating type information regulation 2 homolog-1(Sirt1)to regulate fat deposition of steatotic hepatocyte. The nonalcoholic fatty liver cell model was induced by a mixture of oleic acid and palmitic acid. After successful validation model, the expression of miR-29 a and Sirt1 was measured by PCR. The target genes of miR-29 a was predicted in biological system. MiR-29 a mimic and miR-29 a inhibitor were transfected into hepatocytes, and then established the human steatotic hepatocyte model, the result of oil red O staining and triglyceride(TG)lipid content were observed, the expression of Sirt1 mRNA and protein were detected by qRT-PCR and Western blotting, respectively. The steatosis hepatocyte model was successfully established. Compared with control group, the relative expression of miR-29 a and triglyceride increased significantly(P&lt;0. 01), while the relative expression of Sirt1 decreased significantly(P&lt;0. 01) in the model group. Sirt1 was a target gene of miR-29 a. After transfection, the lipid droplet and the deposition of fat increased obviously in miR-29 a mimic group than those in the control group. TG content in miR-29 a mimic group increased significantly(P&lt;0. 05), the expression of miR-29 a increased significantly(P&lt;0. 01), while the expression of Sirt1 mRNA decreased significantly(P&lt;0. 05), and the expression of Sirt1 protein showed a downtrend. On the contrary, after the inhibition of miR-29 a expression, the lipid droplets in miR-29 a inhibitor group were relatively reduced, the fat deposition was alleviated. The TG content was significantly decreased(P&lt;0. 05), the expression of miR-29 a in the cells was effectively inhibited(P&lt;0. 01), while the expression of Sirt1 mRNA was significantly increased(P&lt;0. 05), and Sirt1 protein was on an upward compared with the control group. The expression of miR-29 a is significantly increased in the nonalcoholic fatty liver cell model. Upregulation of miR-29 a negatively regulates the expression of Sirt1, thus promoting fat deposition of steatotic hepatocyte.

Increased nuclear accumulation of NF-kappaB in LPS-stimulated peripheral blood neutrophils has been shown to be associated with more severe clinical course in patients with infection associated acute lung injury. Such observations suggest that differences in neutrophil response may contribute to the pulmonary inflammation induced by bacterial infection. To examine this question, we sequentially measured LPS-induced DNA binding of NF-kappaB in neutrophils collected from healthy humans on at least three occasions, each separated by at least 2 wk, and then determined pulmonary inflammatory responses after instillation of LPS into the lungs. Consistent patterns of peripheral blood neutrophil responses, as determined by LPS-induced NF-kappaB DNA binding, were present in volunteers, with a >80-fold difference between individuals in the mean area under the curve for NF-kappaB activation. The number of neutrophils recovered from bronchoalveolar lavage after exposure to pulmonary LPS was significantly correlated with NF-kappaB activation in peripheral blood neutrophils obtained over the pre-LPS exposure period (r = 0.65, p = 0.009). DNA binding of NF-kappaB in pulmonary neutrophils also was associated with the mean NF-kappaB area under the curve for LPS-stimulated peripheral blood neutrophils (r = 0.63, p = 0.01). Bronchoalveolar lavage levels of IL-6 and TNFRII were significantly correlated with peripheral blood neutrophil activation patterns (r = 0.75, p = 0.001 for IL-6; and r = 0.48, p = 0.049 for TNFRII. These results demonstrate that stable patterns in the response of peripheral blood neutrophils to LPS exist in the human population and correlate with inflammatory response following direct exposure to LPS in the lung.

This work mainly aimed to explore the role and mechanism of advanced glycation end-products (AGEs) in inducing cerebrovascular endothelial cell pyroptosis under oxygen glucose deprivation (OGD) condition. The mouse cerebral microvascular endothelial cells (BMECs and bEnd.3) were used as the objects to construct the OGD model in vitro. Then, cells were pretreated with AGE-modified human serum albumin (AGE-HSA). Thereafter, CCK-8 assay was conducted to detect cell viability, and flow cytometry (FCM) was performed to measure cell pyroptosis level. Meanwhile, the expression of inflammatory factors was detected by enzyme-linked immunosorbent assay (ELISA). The expression of HIF-α, NLRP3, and RAGE was detected by fluorescence staining. The opening status of cell membrane pore was observed under the electron microscope, and the expression levels of FL-GSDMD, NT-GSDMD, and caspase-1 were measured through Western Blot (WB) assay. Moreover, bEnd.3 cells were treated with siRAN-silenced NLRP3 and HIF-α inhibitor, so as to observe the effect of AGEs on cell pyroptosis level. In the mouse model, the middle cerebral artery occlusion (MCAO) model was constructed by the suture-occluded method. After intraperitoneal injection of AGEs, the pathological changes in mouse brain tissues were detected; the expression levels of NLRP3, ZO-1, and CD31 were determined by histochemical staining, and the levels of inflammatory factors and pyroptosis-related proteins were also detected. Under OGD condition, AGEs induced the pyroptosis of bEnd.3 cells, and the cell pyroptosis rate increased, higher than that of the OGD group. Meanwhile, the levels of inflammatory factors were up-regulated; the expression of HIF-α, NLRP3, and RAGE in cells increased; and the levels of NT-GSDMD and caspase-1 were markedly higher than those of the control and OGD groups. siRNA-NLRP3 or HIF-α inhibitor treatment suppressed pyroptosis and reduced the inflammatory factor levels. In mouse experiments, AGE injection aggravated brain injury in the MCAO mouse model, decreased the expression of ZO-1 and CD31, and elevated the levels of NLRP3 and inflammatory factors. Under cerebral ischemia condition, AGEs can induce endothelial cell pyroptosis via HIF-α-RAGE-NLRP3, thereby further aggravating brain injury.

Atherosclerosis is the leading cause of death from vascular diseases worldwide, and endothelial cell (EC) dysfunction is the key cause of atherosclerosis. miR-155 was found to induce endothelial injury and to trigger atherosclerosis. In addition, brain and muscle ARNT-like protein-1 (Bmal1) has been found to be closely related to EC function. Therefore, the present study aimed to explore the mechanism underlying the regulation of Bmal1 by miR-155 in the induction of EC apoptosis and inflammatory response in atherosclerosis. The atherosclerosis model in apolipoprotein E (ApoE)-/- mice was established. miR-155 and Bmal1 expression was quantified by RT-qPCR and western blot analysis, respectively. The role of miR-155 and Bmal1 in atherosclerosis was evaluated through changes in cardiac function, plaque area, cardiomyocyte apoptosis, and inflammatory factor levels in mice. Moreover, the regulatory relationship between them was identified by dual-luciferase reporter gene assay to explore the mechanism of action of miR-155. After the modeling, the expression of miR-155 was upregulated and Bmal1 was downregulated in aorta, and there was a significant linear correlation between them. Upregulation of miR-155 increased the atherosclerotic plaque area, cell apoptosis, total cholesterol (TC) and triglyceride (TG), as well as weakened aortic diastolic function. However, opposite changes occurred after downregulation of miR-155 or an increase in Bmal1. In addition, the microRNA.org website predicted that there were targeted binding sites between miR-155 and Bmal1, which was verified with a dual-luciferase reporter gene assay. miR-155 was able to inhibit the expression by targeting Bmal1. Moreover, a rescue experiment showed that Bmal1 hindered the promotion of miR-155 in regards to atherosclerosis. In conclusion, miR-155 induces EC apoptosis and inflammatory response, weakens aortic diastolic function, and promotes the progression of atherosclerosis through targeted inhibition of Bmal1.

Ovarian cancer is the most lethal malignancy in female patients, and chemoresistance is the major contribution to low over survival rate. We aim to investigate the correction between Sirt1 expression and chemoresistance in serous epithelial ovarian cancer (EOC) and prognosis significance of Sirt1. Immunochemistry was used to determine the location pattern and expression of Sirt1 in a total of 63 serous EOC patients (28 cases of chemoresistance patients and 35 chemosensitive).The relationship between Sirt1 expression and clinicopathological features of serous EOC was analyzed. Univariate analysis and multifactor logistic regression analysis were applied to investigate risk factor for chemoresistance. Cox proportional hazards regression model and Kaplan-Meier survival analysis were applied to determine the prognosis factor and survival time. Immunohistochemistry proved that over-expression of nuclear Sirt1 was related to chemoresistance (P = 0.039). Multivariate logistic regression analysis proved that the nuclear expression of Sirt1 (P = 0.018) and the lymph node metastasis (P = 0.037) was independent risk factors for chemoresistance in serous epithelial ovarian cancer. Multivariate Cox regression result indicated that expression of Sirt1 (P = 0.026, RR 2.434, 95 % CI 1.109-5.339) and stage (P = 0.005, RR 2.366, 95 % CI 1.288-4.345) was independent prognostic factors. Kaplan-Meier analysis showed that the survival rate is significantly decreased in the Sirt1 highly expressed group. Western blot result showed that the protein level of Sirt1 was significantly higher in chemoresistant group compared with in sensitive group. In conclusion, our results proved that over-expression of Sirt1 could play an important role in chemoresistance of serous EOC and could be a prognosis indicator for the patient's survival outcome.

Chronic kidney disease (CKD) puts patients at a greatly increased risk of cardiovascular disease in a condition termed chronic renocardiac syndrome (RCS). We have utilized the 5/6 nephrectomy (5/6 NX) model in Sprague Dawley rats to study the gradual development of cardiac dysfunction resulting from declining kidney function. Previously, we identified alterations in several microRNAs (miRNAs) in left ventricle (LV) tissue 7 weeks after 5/6 NX surgery. We hypothesized that the upregulation of miR-21 in the LV following 5/6 NX contributes to LV pathology, rather than being a consequence of it. In situ hybridization revealed that miR-21 expression in the LV of 5/6 NX animals is highest in regions of perivascular fibrosis. To study the impact of miR-21 on LV remodeling and function, we delivered locked-nucleic acid (LNA) modified anti-miR-21 or anti-scrambled-miR (Exiqon, delivered i.v. at 1 mg/kg) to 5/6 NX animals (n=6/group) in 3 sequential days at 1 week post-surgery, and again 4 weeks post-surgery. Echocardiography was performed prior to 5/6 NX surgery and bi-weekly thereafter, throughout the 7 week study, to evaluate remodeling and function (anti-miR-21 vs. anti-scramble treated for all comparisons). The average LV miR-21 expression was reduced nearly 12-fold with anti-miR-21 treatment when measured 7 weeks post-5/6 NX. Anti-miR-21 treatment preserved stroke volume and fractional shortening between weeks 3 and 5 post-5/6 NX while both functional indices declined in anti-scramble treated rats. Additionally, concentric LV remodeling (LV wall hypertrophy and reduced chamber diameter) 5 weeks post-5/6 NX was completely prevented with anti-miR-21 treatment. At 7 weeks post-5/6 NX, when LV decompensation is evident in untreated rats, anti-miR-21 treatment maintained LV wall thickness and chamber diameter while fractional shortening was significantly increased (p &lt;0.05). Anti-miR-21 treatment had no effect on blood pressure. We conclude that chronic knockdown of miR-21 in the 5/6 NX model prevented pathological concentric remodeling. Together these data suggest that the upregulation of cardiac miR-21 following 5/6 NX is an important mediator of pathological cardiac remodeling and dysfunction.

Introduction: Shear-sensitive micro-RNAs play an integral role in dictating vascular wall pro-inflammatory response and development of atherosclerosis. Previously, our group and others have identified an inverse relationship between micro-RNA-155 (miR-155) expression and inflammation in atheroprone areas of chronic low magnitude oscillatory shear stress (OSS) in vasculature and in-vitro. Hypothesis: we hypothesized that miR-155 negatively regulates acute OSS-induced vascular inflammation and dysfunction, via modulation of the MAPK-ETS-1 pathway. Methods: 12-week old C57B/6J wild type (WT) and miR-155 knockout mice (KO) were subjected to abdominal aortic coarctation (AAC), a unique model of acute induction of OSS, for 3-7 days. Downstream acute OSS segments were compared to upstream unidirectional shear stress (USS) segments of thoracic aorta using RT-PCR, western blot and two-way ANOVA followed by Tukey’s multiple comparison analyses. Results: In WT mice, acute OSS induced vascular inflammation evidenced by upregulation of MCP-1 and VCAM-1 expression in OSS segments compared with USS. This was associated with loss of vascular barrier function as evaluated by extravasation of Evans-blue dye assay along with increased MMP-9 and MMP-3 expression. However, vascular miR-155 levels were also higher in OSS segments compared with USS (n=6-12, P&lt;0.05). Nevertheless, miR-155 KO mice showed enhanced expression and activation of ERK and p-38 MAPKs and downstream ETS-1, VCAM-1 and MMP-9 expression in OSS segments compared with USS versus WT controls (n=3-4, P&lt;0.05). Tail vein injections of miR-155 overexpressing lentivirus particles in WT mice after AAC resulted in further upregulation of miR-155 and abolished OSS-induced upregulation of p-38 and downstream ETS-1, VCAM-1 and MMP-9 expression in OSS segments compared with USS versus scramble controls (n=5-6, P&lt;0.05). Conclusions: Despite the early upregulation of shear-sensitive miR-155, our data suggest that miR-155 serves as a negative feedback regulator to acute OSS-induced vascular inflammation via inhibition of p-38 and ETS-1. Further studies are in progress to evaluate the effect of exogenous miR-155 on OSS-induced oxidative stress and vascular function, which can serve as basis for developing novel miRNA-based therapeutic modalities.