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Aims/Introduction Materials and Methods Results Conclusions We investigated the relationship of circulating TSP‐1 mRNA and miR‐194 with diabetic kidney disease’s degree.We enrolled 167 hospitalized type 2 diabetes patients in the endocrinology department. Patients were split into three groups according to urinary microalbumin: A, B and C. The control group comprised healthy outpatients (n = 163). The quantities of microribonucleic acid (miR)‐194 and thrombospondin‐1 (TSP‐1) messenger ribonucleic acid (mRNA) in the participants’ circulation were measured using a quantitative real‐time polymerase chain reaction.Circulating TSP‐1 mRNA (P = 0.024) and miR‐194 (P = 0.029) expressions significantly increased in type 2 diabetes patients. Circulating TSP‐1 mRNA (P = 0.040) and miR‐194 (P = 0.007) expression levels differed significantly among the three groups; circulating TSP‐1 mRNA expression increased with urinary microalbumin. However, miR‐194 declined in group B and increased in group C. Circulating TSP‐1 mRNA was positively correlated with cystatin‐c (r = 0.281; P = 0.021) and microalbumin/creatinine ratio (UmALB/Cr; r = 0.317; P = 0.009); miR‐194 was positively correlated with UmALB/Cr (r = 0.405; P = 0.003). Stepwise multivariate linear regression analysis showed cystatin‐c (β = 0.578; P = 0.021) and UmALB/Cr (β = 0.001; P = 0.009) as independent factors for TSP‐1 mRNA; UmALB/Cr (β = 0.005; P = 0.028) as an independent factor for miR194. Areas under the curve for circulating TSP‐1 mRNA and miR194 were 0.756 (95% confidence interval 0.620–0.893; sensitivity 0.69 and specificity 0.71, P < 0.01) and 0.584 (95% confidence interval 0.421–0.748; sensitivity 0.54 and specificity 0.52, P < 0.01), respectively.Circulating TSP‐1 mRNA and miR‐194 expressions significantly increased in type 2 diabetes patients. The microalbumin group had lower levels of miR‐194 (a risk factor that is valuable for type 2 diabetes kidney disease evaluation). [ABSTRACT FROM AUTHOR]

Background and Aim Previous studies have shown differential TIPE2 expression in several autoimmune diseases. However, the expression levels of TIPE2 in primary biliary cirrhosis (PBC) remained unclear. The purposes of this study were to evaluate TIPE2 expression levels in patients with PBC and further investigate its role in PBC pathogenesis. Methods A total of 40 PBC patients and 44 healthy controls were included in the present study. Quantitative reverse-transcription polymerase chain reaction and western blotting were used to determine the differences in mRNA and protein expression levels of TIPE2. The correlations of TIPE2 expression levels and clinical characteristics, inflammatory cytokines, and ursodeoxycholic acid treatment were also assessed. Besides, the influence of TIPE2 on the reactivity of monocyte to Toll-like receptor ligands was further analyzed. Results The expression levels of TIPE2 were significantly decreased in PBC patients compared with normal controls ( P < 0.01). The expression levels of TIPE2 were negatively correlated with alanine aminotransferase ( r = −0.40, P = 0.01), alkaline phosphatase ( r = −0.36, P = 0.02), gamma glutamyl transpeptidase ( r = −0.53, P < 0.01), tumor necrosis factor (TNF)-α ( r = −0.332, P = 0.03), interleukin (IL)-1β ( r = −0.386, P = 0.01), and IL-8 ( r = −0.366, P = 0.02) levels in sera from PBC patients. TIPE2 expression level could be significantly increased after ursodeoxycholic acid treatment ( P < 0.01). The production of TNF-α, IL-1β, and IL-8 by monocytes from PBC patients after stimulation with lipopolysaccharide and lipoteichoic acid was significantly increased when TIPE2 was knocked down. Furthermore, TIPE2 knockdown could promote activation of nuclear factor-κB pathways through increasing phosphorylation and degradation of IκB in peripheral blood monocytes from PBC patients. Conclusion The present study reported that insufficient expression of TIPE2 might be involved in the hyperreactivity of monocyte to Toll-like receptor ligands in PBC. [ABSTRACT FROM AUTHOR]

The transition from liver fibrosis to hepatocellular carcinoma ( HCC) has been suggested to be a continuous and developmental pathological process. Micro RNAs (mi RNAs) are recently discovered molecules that regulate the expression of genes involved in liver disease. Many reports demonstrate that miR-483-5p and miR-483-3p, which originate from miR-483, are up-regulated in HCC, and their oncogenic targets have been identified. However, recent studies have suggested that miR-483-5p/3p is partially down-regulated in HCC samples and is down-regulated in rat liver fibrosis. Therefore, the aberrant expression and function of miR-483 in liver fibrosis remains elusive. In this study, we demonstrate that overexpression of miR-483 in vivo inhibits mouse liver fibrosis induced by CCl4. We demonstrate that miR-483-5p/3p acts together to target two pro-fibrosis factors, platelet-derived growth factor-β and tissue inhibitor of metalloproteinase 2, which suppress the activation of hepatic stellate cells ( HSC) LX-2. Our work identifies the pathway that regulates liver fibrosis by inhibiting the activation of HSCs. [ABSTRACT FROM AUTHOR]

In the past several years, microRNAs have been identified as a class of important regulators of gene expression. One hot topic in the microRNA field is the location of microRNA genes. Most microRNAs are called intronic microRNAs, which are encoded in the introns of coding or non-coding genes. Some research studies have shown that intronic miRNAs coexpress and act similarly to their host genes; however, other research studies have suggested that their level of expression and function are opposite to that of their host genes. Intronic microRNAs have been reported to play an antagonistic or synergetic role as an enemy or a partner of their host genes. Elucidation of the relationship between intronic microRNAs and their host genes will facilitate a deeper understanding of gene expression and the function of introns. This mini review will discuss recent research addressing intronic microRNAs and their host genes. © 2012 IUBMB IUBMB Life, 64(10): 835-840, 2012 [ABSTRACT FROM AUTHOR]

Abstract: Angiogenesis, a key factor in ischemic heart disease, is rapidly initiated in response to hypoxic or ischemic conditions. MicroRNAs (miRNAs) are endogenously expressed small non-coding RNAs that regulate gene expression at post-transcriptional level. The recent discovery of the involvement of these RNAs in the control of angiogenesis renders them very attractive in the development of new approaches for restoring the angiogenic balance. In the present study, we explored that miR-483-5p, a microRNA embedded in the intron of insulin-like growth factor 2 (Igf2), acts as an endogenous angiogenesis-inhibiting factor. We identified that serum response factor (SRF) is one of miR-483-5p target genes. These findings indicated that the miR-483-5p-SRF pathway may offer a novel strategy for treatment with angiogenesis in ischemic heart disease patients. [Copyright &y& Elsevier]