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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]

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]

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]