Expression of miR-155, miR-146a, and miR-326 in T1D patients from Chile: relationship with autoimmunity and inflammatory markers

García-Díaz, Diego F.; Pizarro, Carolina; Camacho-Guillén, Patricia; Codner, Ethel; Soto, Néstor; Pérez-Bravo, Francisco

doi:10.20945/2359-3997000000006

Cited by 23 publications

(17 citation statements)

References 31 publications

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“…Another study has also pointed out that miR-495 affects the occurrence of mandatory spondylitis through the targeted inhibition of DVL-2( 31 ) and the study by Tomofuji et al ( 32 ) has also confirmed that miR-495 may be a potential marker of periodontitis. Similarly, a previous study has suggested that miR-326 may be closely related to RA in diabetic patients ( 33 ). All the aforementioned studies have shown that miR-495 and miR-326 are closely related to bone diseases and therefore, it is of great significance to continue to explore miR-495 and miR-326 in RA.…”

Section: Discussionsupporting

confidence: 54%

Expression of miR‑495 and miR‑326 in peripheral blood of rheumatoid arthritis patients and its significance

2020

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The aim of the present study was to investigate the expression of microRNA (miR)-495 and miR-326 in the peripheral blood of patients with rheumatoid arthritis (RA). A total of 107 RA patients, admitted to the Yidu Central Hospital of Weifang (Weifang, China) from February 2016 to February 2019, and 112 healthy subjects, who underwent physical examination during the same period, were selected as the research subjects for prospective analysis. The RA patients served as the study group and the healthy subjects as the control group. The expression levels of miR-495 and miR-326 in the peripheral blood of the two groups of subjects were compared. The association between miR-495 and miR-326 with RA clinical pathology and the diagnostic value of miR-495 and miR-326 for RA were analyzed. In the study group, miR-495 expression was significantly higher than that in the control group, and miR-326 expression was significantly lower than that in the control group (P<0.001). miR-495 and miR-326 combined diagnosis showed good predictive value for the occurrence of RA (P<0.001) and was closely related to RA clinical pathology (P<0.001). After treatment, miR-495 expression was significantly decreased in the study group, whereas miR-326 expression was significantly increased (P<0.001). Pearson's correlation coefficient analysis showed that rheumatoid factor (RF) was positively correlated with miR-495 expression and negatively correlated with miR-326 expression (P<0.001). In conclusion, miR-495 was highly expressed in patients with RA, whereas miR-326 was poorly expressed in RA patients, and the combined detection of miR-495 and miR-326 has good diagnostic value for RA.

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Section: Discussionsupporting

confidence: 54%

Expression of miR‑495 and miR‑326 in peripheral blood of rheumatoid arthritis patients and its significance

2020

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“…A literature search provided evidence that 20 of these miRNAs are associated with diabetes and/or cardiac fibrosis and/or different cardiovascular diseases (Table 2). The microRNA miR-155-5p, a biomarker that is increased in the plasma of patients with type 1 diabetes [31, 32] and in gingival crevicular fluid of patients with periodontitis and type 2 diabetes [33] and contributes to cardiac hypertrophy and coronary heart disease [34, 35], was increased by 5.21-fold in the ZO rat heart, consistent with the cardiovascular detrimental effects of diabetes. Other miRNAs that have defined roles in cardiovascular damage included miR-872-5p, miR-350, miR-362-3p, miR-223-3p, miR-204, miR-98, miR-217, miR-379, and miR-181-3p (Table 2 and references therein).…”

Section: Resultsmentioning

confidence: 93%

Comparison of Cardiac miRNA Transcriptomes Induced by Diabetes and Rapamycin Treatment and Identification of a Rapamycin-Associated Cardiac MicroRNA Signature

Belenchia

Gavini²,

Toedebusch

et al. 2018

Oxidative Medicine and Cellular Longevity

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Rapamycin (Rap), an inhibitor of mTORC1, reduces obesity and improves lifespan in mice. However, hyperglycemia and lipid disorders are adverse side effects in patients receiving Rap treatment. We previously reported that diabetes induces pansuppression of cardiac cytokines in Zucker obese rats (ZO-C). Rap treatment (750 μg/kg/day for 12 weeks) reduced their obesity and cardiac fibrosis significantly; however, it increased their hyperglycemia and did not improve their cardiac diastolic parameters. Moreover, Rap treatment of healthy Zucker lean rats (ZL-C) induced cardiac fibrosis. Rap-induced changes in ZL-C's cardiac cytokine profile shared similarities with that of diabetes-induced ZO-C. Therefore, we hypothesized that the cardiac microRNA transcriptome induced by diabetes and Rap treatment could share similarities. Here, we compared the cardiac miRNA transcriptome of ZL-C to ZO-C, Rap-treated ZL (ZL-Rap), and ZO (ZO-Rap). We report that 80% of diabetes-induced miRNA transcriptome (40 differentially expressed miRNAs by minimum 1.5-fold in ZO-C versus ZL-C; p ≤ 0.05) is similar to 47% of Rap-induced miRNA transcriptome in ZL (68 differentially expressed miRNAs by minimum 1.5-fold in ZL-Rap versus ZL-C; p ≤ 0.05). This remarkable similarity between diabetes-induced and Rap-induced cardiac microRNA transcriptome underscores the role of miRNAs in Rap-induced insulin resistance. We also show that Rap treatment altered the expression of the same 17 miRNAs in ZL and ZO hearts indicating that these 17 miRNAs comprise a unique Rap-induced cardiac miRNA signature. Interestingly, only four miRNAs were significantly differentially expressed between ZO-C and ZO-Rap, indicating that, unlike the nondiabetic heart, Rap did not substantially change the miRNA transcriptome in the diabetic heart. In silico analyses showed that (a) mRNA-miRNA interactions exist between differentially expressed cardiac cytokines and miRNAs, (b) human orthologs of rat miRNAs that are strongly correlated with cardiac fibrosis may modulate profibrotic TGF-β signaling, and (c) changes in miRNA transcriptome caused by diabetes or Rap treatment include cardioprotective miRNAs indicating a concurrent activation of an adaptive mechanism to protect the heart in conditions that exacerbate diabetes.

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“…Recently, the miRNAs-NF-κB pathway has been considered as a new target for manipulating and preventing the concomitant diabetic-induced conditions [ 26 ]. The decreased miRNA‐146 expression has been reported in peripheral blood mononuclear cells of patients with type-I diabetes [ 27 , 28 ], and endothelial cells of mice [ 29 ]. Similarly, in this study, the improving effects of troxerutin on inflammatory reactions and intercellular adhesion molecules were associated with enhanced expression of miRNA-146a in aortic tissue of type-I diabetic rats.…”

Section: Discussionmentioning

confidence: 99%

Effects of troxerutin on vascular inflammatory mediators and expression of microRNA-146a/NF-κB signaling pathway in aorta of healthy and diabetic rats

Xing

Dai

2020

Korean J Physiol Pharmacol

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This study has investigated the effect of a potent bioflavonoid, troxerutin, on diabetes-induced changes in pro-inflammatory mediators and expression of microRNA-146a and nuclear factor-kappa-B (NF-κB) signaling pathway in aortic tissue of type-I diabetic rats. Male Wistar rats were randomly divided into four groups (n = 6/each): healthy, healthy-troxerutin, diabetic, and diabetic-troxerutin. Diabetes was induced by streptozotocin injection (60 mg/kg; intraperitoneally) and lasted 10 weeks. Troxerutin (150 mg/kg/day) was administered orally for last month of experiment. Inflammatory cytokines IL-1, IL-6, and TNF-, as well as intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule (VCAM), cyclooxygenase-II (COX-II), and inducible-nitric oxide synthase (iNOS) were measured on aortic samples by enzyme-linked immunosorbent assay. Gene expressions for transcription factor NF-κB, interleukin-1 receptor-associated kinase-1 (IRAK-1), TNF receptor-associated factor-6 (TRAF-6), and microRNA-146a were determined using real-time polymerase chain reaction. Ten-week diabetes significantly increased mRNA levels of IRAK-1, TRAF-6, NF-κB, and protein levels of cytokines IL-1, IL-6, TNF-, adhesion molecules ICAM-1, VCAM, and iNOS, COX-II, and decreased expression of microRNA-146a as compared with healthy rats (p < 0.05 to p < 0.01). However, one month treatment of diabetic rats with troxerutin restored glucose and insulin levels, significantly decreased expression of inflammatory genes and pro-inflammatory mediators and increased microRNA level in comparison to diabetic group (p < 0.05 to p < 0.01). In healthy rats, troxerutin had significant reducing effect only on NF-κB, TNF- and COX-II levels (p < 0.05). Beside slight improvement of hyperglycemia, troxerutin prevented the activation of NF-κB-dependent inflammatory signaling in the aorta of diabetic rats, and this response may be regulated by microRNA-146a.

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Expression of miR-155, miR-146a, and miR-326 in T1D patients from Chile: relationship with autoimmunity and inflammatory markers

Cited by 23 publications

References 31 publications

Expression of miR‑495 and miR‑326 in peripheral blood of rheumatoid arthritis patients and its significance

Expression of miR‑495 and miR‑326 in peripheral blood of rheumatoid arthritis patients and its significance

Comparison of Cardiac miRNA Transcriptomes Induced by Diabetes and Rapamycin Treatment and Identification of a Rapamycin-Associated Cardiac MicroRNA Signature

Effects of troxerutin on vascular inflammatory mediators and expression of microRNA-146a/NF-κB signaling pathway in aorta of healthy and diabetic rats

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