OBJECTIVE: To summarize the regulatory effect of non-coding RNA (ncRNA) on type H vessels angiogenesis of bone. METHODS: Recent domestic and foreign related literature about the regulation of ncRNA in type H vessels angiogenesis was widely reviewed and summarized. RESULTS: Type H vessels is a special subtype of bone vessels with the ability to couple bone formation. At present, the research on ncRNA regulating type H vessels angiogenesis in bone diseases mainly focuses on microRNA, long ncRNA, and small interfering RNA, which can affect the expressions of hypoxia inducible factor 1α, platelet derived growth factor BB, slit guidance ligand 3, and other factors through their own unique ways of action, thus regulating type H vessels angiogenesis and participating in the occurrence and development of bone diseases. CONCLUSION At present, the mechanism of ncRNA regulating bone type H vessels angiogenesis has been preliminarily explored. With the deepening of research, ncRNA is expected to be a new target for the diagnosis and treatment of vascular related bone diseases.
Humans ; RNA, Untranslated/genetics* ; RNA, Long Noncoding ; Bone Diseases/genetics* ; MicroRNAs/genetics* ; RNA, Small Interfering

Animals ; Humans ; MicroRNAs ; physiology ; RNA, Small Interfering ; physiology ; RNA, Untranslated ; physiology

High-throughput RNA-seq has revolutionized the process of small RNA (sRNA) discovery, leading to a rapid expansion of sRNA categories. In addition to the previously well-characterized sRNAs such as microRNAs (miRNAs), piwi-interacting RNAs (piRNAs), and small nucleolar RNA (snoRNAs), recent emerging studies have spotlighted on tRNA-derived sRNAs (tsRNAs) and rRNA-derived sRNAs (rsRNAs) as new categories of sRNAs that bear versatile functions. Since existing software and pipelines for sRNA annotation are mostly focused on analyzing miRNAs or piRNAs, here we developed the sRNA annotation pipelineoptimized for rRNA- and tRNA-derived sRNAs (SPORTS1.0). SPORTS1.0 is optimized for analyzing tsRNAs and rsRNAs from sRNA-seq data, in addition to its capacity to annotate canonical sRNAs such as miRNAs and piRNAs. Moreover, SPORTS1.0 can predict potential RNA modification sites based on nucleotide mismatches within sRNAs. SPORTS1.0 is precompiled to annotate sRNAs for a wide range of 68 species across bacteria, yeast, plant, and animal kingdoms, while additional species for analyses could be readily expanded upon end users' input. For demonstration, by analyzing sRNA datasets using SPORTS1.0, we reveal that distinct signatures are present in tsRNAs and rsRNAs from different mouse cell types. We also find that compared to other sRNA species, tsRNAs bear the highest mismatch rate, which is consistent with their highly modified nature. SPORTS1.0 is an open-source software and can be publically accessed at https://github.com/junchaoshi/sports1.0.
Animals ; Gene Expression Profiling ; High-Throughput Nucleotide Sequencing ; Mice ; MicroRNAs ; chemistry ; metabolism ; Molecular Sequence Annotation ; RNA, Ribosomal ; chemistry ; metabolism ; RNA, Small Interfering ; chemistry ; metabolism ; RNA, Small Untranslated ; chemistry ; metabolism ; RNA, Transfer ; chemistry ; metabolism ; Sequence Analysis, RNA ; methods ; Software

It has been shown that CA repeats in the 3'-untranslated region (UTR) of bcl-2 mRNA contribute the constitutive decay of bcl-2 mRNA and that hnRNP L (heterogenous nuclear ribonucleoprotein L) interacts with CA repeats in the 3'-UTR of bcl-2 mRNA, both in vitro and in vivo. The aim of this study was to determine whether the alteration of hnRNP L affects the stability of bcl-2 mRNA in vivo. Human breast carcinoma MCF-7 cells were transfected with hnRNP L-specific shRNA or hnRNP L-expressing vector to decrease or increase hnRNP L levels, respectively, followed by an actinomycin D chase. An RT-PCR analysis showed that the rate of degradation of endogenous bcl-2 mRNA was not affected by the decrease or increase in the hnRNP L levels. Furthermore, during apoptosis or autophagy, in which bcl-2 expression has been reported to decrease, no difference in the degradation of bcl-2 mRNA was observed between control and hnRNP L-knock down MCF-7 Cells. On the other hand, the levels of AUF-1 and nucleolin, transacting factors for ARE in the 3'UTR of bcl-2 mRNA, were not significantly affected by the decrease in hnRNP L, suggesting that a disturbance in the quantitative balance between these transacting factors is not likely to interfere with the effect of hnRNP L. Collectively, the findings indicate that the decay of bcl-2 mRNA does not appear to be directly controlled by hnRNP L in vivo.
3' Untranslated Regions ; Apoptosis ; Autophagy ; Breast ; Dactinomycin ; Hand ; Heterogeneous-Nuclear Ribonucleoprotein L ; Heterogeneous-Nuclear Ribonucleoproteins ; Humans ; MCF-7 Cells ; Phosphoproteins ; Ribonucleoproteins ; RNA, Messenger ; RNA, Small Interfering ; RNA-Binding Proteins

OBJECTIVETo evaluate interfering effect of several short interfering RNAs (siRNA) on HCV 5' untranslated region(5' UTR).

METHODSThe green fluorescent protein (GFP) was used as reporter gene. A fused gene of HCV-5'UTR and GFP was constructed. It was cloned into the plasmid pCDNA3.1 named as pcDNA-HCV-5'UTR-GFP. Three siRNAs were designed and transfected into HepG2 cells with pcDNA-HCV-5'UTR-GFP. The change of the fluorescence intensity of HepG2 cells was shown by fluorescence microscopy and numerically detected under 488 nm wave length by flow cytometry.

RESULTSThe fused gene of HCV-5'UTR and GFP was successfully constructed. The seven groups displayed inhibitory effects on the gene expression of GFP. The inhibition rates of siRNA A, B and C were 68.4 percent, 72.6 percent and 75.6 percent, respectively. The inhibitory rates of siRN A + B, siRN B +C and siRN A +C were 91.8 percent, 87.2 percent and 92.4 percent, respectively. The inhibitory rates of siRN A+B +C was the highest, up to 95.7 percent.

CONCLUSIONThese siRNAs could inhibit expression of HCV 5'UTR gene, the inhibitory effect of combined siRNA was better than that of single siRNAs.

5' Untranslated Regions ; genetics ; Green Fluorescent Proteins ; genetics ; Hepacivirus ; genetics ; RNA Interference ; RNA, Small Interfering ; genetics ; Transfection

OBJECTIVETo explore whether miR-200b suppresses tumor cell invasion by targeting PROM1, thus to reveal the molecular mechanism that miR-200b functions as a tumor suppressor in glioma.

METHODSPROM1 3'UTR-luciferase vector was constructed and dual-luciferase reporter gene assay was employed to examine the effect of miR-200b on luciferase activity. Human glioblastoma U87 cells were transfected with miR-200b mimics, and next qRT-PCR and Western blotting were performed to detect the expressions of PROM1 mRNA and protein. The effect of PROM1 down-regulation on invasion was observed after PROM1 siRNA were transfected into U87 cells.

RESULTSThe miR-200b bound to the 3'-untranslated region (UTR) of PROM1 and inhibited the luciferase activity. Its luciferase activity was down-regulated by 57.0% (P < 0.01). PROM1 protein and mRNA expressions were significantly down-regulated when miR-200b was overexpressed in the U87 cells (P < 0.05). siRNA-mediated down-regulation of PROM1 suppressed the potential of cell invasion. The invasion ability of SKOV3 cells after transfection with siRNA-PROM1 was significantly lower than that in the negative control cells (P < 0.05).

CONCLUSIONmiR-200b may suppress cell invasion by targeting PROM1 in glioma.

3' Untranslated Regions ; AC133 Antigen ; Antigens, CD ; metabolism ; Cell Line, Tumor ; Down-Regulation ; Genes, Reporter ; Genes, Tumor Suppressor ; Genetic Vectors ; Glioblastoma ; genetics ; metabolism ; Glycoproteins ; metabolism ; Humans ; Luciferases ; MicroRNAs ; metabolism ; Peptides ; metabolism ; RNA, Messenger ; RNA, Small Interfering ; Transfection

Animals ; Apoptosis ; Cadherins ; genetics ; metabolism ; Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs ; genetics ; metabolism ; physiology ; Neoplasm Invasiveness ; Neoplasms ; genetics ; metabolism ; pathology ; therapy ; RNA, Double-Stranded ; genetics ; metabolism ; physiology ; RNA, Small Interfering ; genetics ; metabolism ; physiology ; RNA, Small Untranslated ; genetics ; metabolism ; physiology ; therapeutic use ; Transcriptional Activation

PURPOSE: MicroRNAs are small noncoding RNAs and microRNA-214 (miR-214) has been associated with the inhibition of cancer cell growth, migration, and invasion. The aim of this study was to investigate whether cell-free miR-214 isolated from urine could be used as a biomarker for non-muscle-invasive bladder cancer (NMIBC). MATERIALS AND METHODS: A total of 138 patients with primary NMIBC and 144 healthy normal controls were enrolled in this study. By use of quantitative polymerase chain reaction (PCR), the urinary levels of cell-free miR-214 were measured and the clinicopathological parameters of patients with NMIBC were compared with those of the controls. RESULTS: The urinary levels of cell-free miR-214 were significantly higher in the NMIBC patients than in the controls (20.08+/-3.21 vs. 18.96+/-2.68, p=0.002). However, the urinary levels of cell-free miR-214 were neither graded nor staged for the NMIBC patients (p>0.05, each). When we compared the urinary levels of cell-free miR-214 according to clinical outcomes, patients with recurrence had lower levels of miR-214 than did those with no recurrence (19.24+/-2.67 vs. 20.41+/-3.41, p=0.023). By contrast, there were no significant differences in the urinary level of cell-free miR-214 between the NMIBC patients showing progression and those showing no progression (p=0.919). Multivariate Cox regression analysis revealed that urinary levels of cell-free miR-214 were an independent predictor of NMIBC recurrence (hazard ratio, 2.011; 95% confidence interval, 1.027 to 3.937; p=0.041). CONCLUSIONS: Urinary levels of cell-free miR-214 could be an independent prognostic parameter for NMIBC recurrence. Thus, urinary cell-free microRNA-214 might be a useful prognostic marker for NMI BC.
Humans ; MicroRNAs ; Polymerase Chain Reaction ; Recurrence ; RNA, Small Untranslated ; Urinary Bladder Neoplasms* ; Urinary Bladder*

Adipocyte differentiation, termed adipogenesis, is a complicated process in which pluripotent mesenchymal stem cells differentiate into mature adipocytes. The process of adipocyte differentiation is tightly regulated by a number of transcription factors, hormones and signaling pathway molecules. Recent studies have demonstrated that microRNAs, which belong to small noncoding RNA species, are also involved in adipocyte differentiation. In vivo and in vitro studies have revealed that various microRNAs affect adipogenesis by targeting several adipogenic transcription factors and key signaling molecules. In this review, we will summarize the roles of microRNAs in adipogenesis and their target genes associated with each stage of adipocyte differentiation.
Adipocytes* ; Adipogenesis ; Mesenchymal Stromal Cells ; MicroRNAs* ; Obesity ; RNA, Small Untranslated ; Transcription Factors

Since the first descriptions of their active functions more than ten years ago, small non-coding RNA species termed microRNA (miRNA) have emerged as essential regulators in a broad range of adaptive and maladaptive cellular processes. With an exceptionally rapid pace of discovery in this field, the dysregulation of many individual miRNAs has been implicated in the development and progression of various cardiovascular diseases. MiRNA are also expected to play crucial regulatory roles in the progression of pulmonary vascular diseases such as pulmonary hypertension (PH), yet direct insights in this field are only just emerging. This review will provide an overview of pulmonary hypertension and its molecular mechanisms, tailored for both basic scientists studying pulmonary vascular biology and physicians who manage PH in their clinical practice. We will describe the pathobiology of pulmonary hypertension and mechanisms of action of miRNA relevant to this disease. Moreover, we will summarize the potential roles of miRNA as biomarkers and therapeutic targets as well as future strategies for defining the cooperative actions of these powerful effectors in pulmonary vascular disease.
Anoxia ; Biomarkers ; Biology ; Cardiovascular Diseases ; Hydrogen-Ion Concentration ; Hypertension, Pulmonary ; MicroRNAs ; RNA, Small Untranslated ; Vascular Diseases