Background: Carotid disease is one of the many forms of cardiovascular disease, which may lead to chronic disability and death. It is a multifactorial inflammatory disease, greatly affected by an individual’ s habits like smoking, lack of exercise, and a diet high in fats. MicroRNAs (miRs) are known to be involved in vascular inflammation. Objectives: We aimed to analyse in a case-control study the expression profile of selected miRs from patients with symptomatic carotid disease and to examine their involvement in the disease pathogenesis. Patients and Methods: Samples from 38 symptomatic patients who underwent carotid endarterectomy were collected and adjacent healthy regions from 15 patients were used as control samples. Fold change in the expression of miR21, miR122, miR146a and miR196α was measured using reverse transcription-real time PCR. Western blot was used to quantify the levels of MMP2 protein whose gene is a target of miR21. Results: Compared to control samples, all patients showed upregulation of miR21, miR122, miR146a and miR196a. No statistical significance was found to exist from patients with high or low miRs expression and clinical/laboratory parameters. The levels of MMP2 were found to be decreased in patients when compared to control samples. Conclusions: Our results revealed miRs which showed different expression in endarterectomy specimens from patients with symptomatic carotid disease, suggesting that these miRs correlated with vascular inflammation. Furthermore, miR21 seems an appealing pharmaceutical target since by targeting MMP2 can favour a stable plaque since low levels of the protein of its gene MMP2 target prevent the fibrous cap of the atheroma from getting thinner. Thus, miR21 seems to prevent rupture but further research is required.

Objective(s): MicroRNA-21 (miR21) is aberrantly elevated in rheumatoid arthritis (RA) patients, the significance of this microRNA in RA pathogenesis and treatment, however, has not been investigated. In this study, by using RA-derived fibroblast-like synoviocyte (FLS) cells as a model, we investigated the effect and corresponding mechanism of miR21 inhibition on FLSs invasion. Materials and Methods: miR21 expression in synovial tissue and FLSs in RA patients and non-RA controls were determined by stem-loop RT-PCR. The effect of miR21 on FLSs viability and invasiveness were evaluated using miR21 inhibition. Cell viability was evaluated by MTT assay and the expression of genes at mRNA and protein levels was determined by RT-PCR and Western blot, respectively. Results: Our results showed that miR21 expression was highly increased in synovial tissue and FLSs in RA patients. Also, we reported that miR21 inhibitor treatment could significantly suppress the invasiveness of FLSs without affecting cell viability. The decreased FLSs invasion by miR21 inhibition was associated with down-regulated expression of matrix metalloproteinase (MMP)-1, MMP3, and MMP13. Further analysis revealed that miR21 inhibition could suppress the expression of TGFβ 1 and Smad4, but promote that of Smad7. Moreover, suppression of FLS invasion and MMPs expression by miR21 treatment could be counteracted by additional TGFβ 1 treatment. Conclusion: Our results indicated that miR21 inhibition can down-regulate the expression of MMP1, MMP3, and MMP13 and consequently suppress the invasiveness of FLS, which is achieved through TGFβ 1/Smad4/7 signaling pathway. The findings of this study could offer a novel approach for RA treatment.

Background: Micro-RNAs (miRs) play several roles during infections with viruses. Therefore, the roles of miR21 and mir155 in the induction of the viral-related cancers have been the focus of attention in several studies. High risk human papilloma viruses (HPVs) are the main factors negatively contributing to the induction of HPV-related cancers. This study aimed to evaluate the expression of miR21 and mir155 in the patients with HPV-high risk genotypes in order to explore the roles of the miRs in the induction of HPVrelated cancers. Methods: In this study, 40 women infected with the high-risk HPV genotypes as well as 40 healthy controls were examined regarding the relative expression of miR21 and mir155 by adopting real-time polymerase chain reaction (PCR) technique. U6 was used for data normalization of miRNAs. Results: Relative expressions of both miR21 and miR155 were significantly higher in the HPV-infected patients compared to those in non-infected women. Conclusions: It was concluded that miR21 and miR155 may have played key roles in the induction of HPVrelated cancers among Iranian patients.

Hepatitis B virus (HBV) X protein (HBx) plays a key role in hepatocellular carcinoma (HCC). HBx may alter the expression of multiple microRNAs (miRs), which are important in hepatocarcinogenesis. This study aimed to investigate the importance of HBx protein in the expression of miR-21, miR-22, miR-122, miR-132, and miR-222. A recombinant vector expressing HBx was developed. The Huh-7 cell line was transfected with the HBx-pcDNA3. 1+ recombinant plasmid. A Real-Time Polymerase Chain Reaction was used to evaluate the expression of miR-21, miR-22, miR-122, miR-132, and miR-222 in the cell line. It was found that the expression of miR-21 and miR-222 was upregulated at all points of time after HBx transfection. The expression of miR-21 was 4. 24-fold 72 h after transfection. The miR-22 had a 7. 69-fold downregulation after 24 h, and the miR-122 had a significant downregulation after 48 h (10-fold). The miR-132 expression reached its lowest rate 12 h after HBx transfection (8. 33-fold), and the miR-222 expression was upregulated in transfected cells but was not significantly different (1. 18-to 2. 45-fold). The significant downregulation of miR-22, miR-122, and miR-132 implicates their inhibitory roles in the progression of HBV-associated HCC. The expression of these microRNAs could be used as a prognostic marker for the progression of HBV-associated liver disease

Introduction. Chronic allograft nephropathy is characterized by interstitial fibrosis and tubular atrophy. The main players in the process of fibrosis are transforming growth factor-β (TGF-β ) and miR-21 expression with a bidirectional interplay. This study aimed to evaluate the effects of angiotensin receptor type 1 antagonist, losartan, on peripheral blood and tissue expression of TGF-β and miR-21 and histologic findings in allograft biopsy in kidney transplant recipients. Materials and Methods. In a randomized controlled trial, 54 patients were enrolled and divided randomly into 2 groups. Group 1 was treated with a daily dose of 25 mg of losartan and group 2 was considered as control. Blood sampling was done at 48 hours posttransplantation and the 3rd and 6th months after transplantation for measurement of TGF-β RNA and miR-21. Protocol biopsy was performed at the 6th month posttransplantation for RNA extraction and histologic evaluation of interstitial fibrosis and tubular atrophy. Results. Although patients were not different initially, those who underwent treatment with losartan had lower miR-21 and TGF-β levels in circulating PBMCs, and there was a decreasing trend in peripheral blood TGF-β levels during the 6-month follow-up period. Tissue expression of miR-21 and TGF-β was also considerably lower among the losartan-treated patients at the time of tissue biopsy. Conclusions. Losartan treatment decreased the tissue expression of miR-21 and TGF-β and tissue fibrosis in kidney transplant patient, and it had a protective effect on allograft function and may delay chronic allograft dysfunction by reducing mediators of fibrosis.

Breast cancer is the most common cause of death from cancer among women. The triple-negative breast cancer (TNBC) is the most invasive subtype, and chemotherapy is the only therapy option. Cancer cells preferably utilize the glycolysis pathway even with proper oxygen availability, and this activation plays a great role in tumorigenesis. Therefore, glycolysis targeting can be an effective strategy for cancer treatment. Here, the apoptotic effect of a glycolysis inhibitor named dichloroacetate (DCA) on TNBC cells MDA-MB-231 was assessed, and the expression of anti-apoptotic genes and oncogenic miRNAs was evaluated. MTT assay showed that DCA reduces cell viability in a dose-dependent manner with the IC50 concentration of 50 mM. Annexin/PI assay demonstrated that DCA due to DCA treatment. Finally, the expression of anti-apoptotic genes Bcl2l1 and Mcl1 and oncogenic miRNAs miR21 and miR27a decreased due to DCA treatment. Our results confirmed that DCA, as a glycolysis inhibitor, leads to apoptosis induction in TNBC cells because of reducing expression of viability genes and miRNAs.