Long non-coding RNAs (lncRNAs) have been demonstrated to be significant in numerous biological processes. Hypertension is a form of cardiovascular disease with at least one billion cases worldwide. The present study sought to compare the differential expression profiles of lncRNAs in the renal cortex of spontaneously hypertensive rats (SHRs) and normotensive Wistar‑Kyoto (WKY) rats. The ipsilateral renal cortex was obtained from 15‑week‑old SHRs and WKY rats whose blood pressures had been monitored. Total RNA was extracted using TRIzol, and lncRNAs and messenger RNAs were profiled by microarray and validated using fluorescent quantitative reverse transcription‑polymerase chain reaction. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to predict the function of differentially expressed genes. Microarray analysis demonstrated that 145 lncRNAs were differentially expressed between SHRs and WKY rats. GO and KEGG pathway analysis indicated that these lncRNAs are involved in numerous biological processes. Thus, lncRNAs may contribute to the pathogenesis of hypertension.

OBJECTIVE:To investigate the effects of angiotensin II (Ang II) antagonist telmisartan on retina vessel endothelial cell apoptosis and its impact on the ACE2-Ang-(1-7)-Mas axis in spontaneous hypertensive rats (SHR). METHODS:Thirty-six SHR 16 week-old were randomly divided into 3 groups (n = 12 each): SHR, SHRT (telmisartan 10 mg · kg-1 · d-1 by gastric gavage) and SHRTA group (telmisartan 10 mg · kg-1 · d-1 by gastric gavage plus intravenous injection of A-779 0.5 mg · kg-1 · d-1), twelve WKY rats served as normotensive control group. Systolic blood pressure was measured at pre-treatment and 8 weeks later. After 8 weeks, rats were sacrificed, the expression of ACE2 and Mas in retina were analyzed by qRT-PCR, Western blot and Immunohistochemistry, the Ang-(1-7) concentration in serum was measured by ELISA. Specimens were obtained and stained by hematoxylin and eosin, and the morphology of retina vessel was observed. Apoptosis of vessel endothelial cells were determined by using terminal deoxynucleotidyl transferase mediated dUTP nick end labeling method. RESULTS:The systolic blood pressure of SHR, SHRT and SHRTA groups at baseline were significantly higher than age-matched WKY group (all P < 0.01). Eight weeks later, the systolic blood pressure group was significantly lower in SHRT group than in the SHR group (P < 0.01), this effect was partly reversed in SHRTA group. The retinal ACE2 mRNA and protein expression was significantly lower in SHR group than in WKY and SHRT groups (P < 0.01), which was similar between SHRT group and SHRTA group (P > 0.05). The retinal Mas mRNA and protein expression were significantly lower in SHR group compared to WKY and SHRT groups (all P < 0.01), which was significantly lower in SHRTA group than in the SHRT group (P < 0.05). ELISA results showed that serum Ang-(1-7) protein level was significantly lower in SHR group than in WKY group and SHRT group (both P < 0.05), which was lower in SHRTA group compared to SHRT group. Retinal vessel endothelial cell apoptosis was higher in SHR group than in WKY group, which could be reduced by cotreatment with telmisartan and this beneficial effect could be reversed by A-779. CONCLUSION:Telmisartan can reduce retinal vessel endothelial cell apoptosis via upregulating the ACE2-Ang-(1-7)-Mas axis.

Objective:Pax-8 gene plays a pivotal role in embryonic development and tumorgenesis. This study aims to identify and clone different alternatively splicing isoforms of mouse Pax-8, and to detect their spa-tial and temporal expression patterns. Methods:Hearts from wild-type prenatal and postnatal mice of C57BL/6 background were carefully excised and total RNA was extracted using Trizol reagent. The cDNA fragment of Pax-8 was reverse transcribed and ampliifed by Q5 Taq polymerase and cloned into pcDNA3.1(-) vector. The re-combinant vectors were validated by enzyme digestion and sequencing. Results:In comparison to their cognate full-length Pax-8a, three alternatively splicing isoforms of mouse Pax-8, designated Pax-8b (exon4 deleted), Pax-8c (exon 4 and 11 deleted) and Pad-8d (exon 4 and 9 deleted), were identiifed in different periods of embryogen-esis and successfully cloned. Conclusion:Mouse heart has four alternatively splicing isoforms of mouse Pax-8 that express in different spatial and temporal expression patterns. Such ifndings open a bright avenue for the further functional study.

Objective:To clone mouse orphan nuclear receptors(NR4A1) full-length cDNA and construct its recombinant eukaryotic expression vector for the preparation to study its function in cardiomyocytes.Methods: The total RNA from Pax-8 knockout mice cardiac tissue was extracted.The cDNA was amplified by semi-quantitative PCR before inserted into pGEM-T Easy vector and confirmed by sequence analysis.The pGEM-T Easy vector which contained NR4A1 cDNA was amplified by PCR.The pIERS2-ZsGreen1 vector which contained NR4A1 cDNA was cloned and constructed.The recombinant vector pIERS2-ZsGreen1-NR4A1 was transfected into H9C2 cardiomyocytes by Lipofectamine2000.The level of expression of NR4A1 mRNA and protein was assayed with RT-PCR and Western blotting.The experiment was divided into three groups: the PZ-NR4A1 group was transfected with 1.2μg pIERS2-ZsGreen1-NR4A1 recombinant vector,the NC group was transfected with 1.2μg pIERS2-ZsGreen1 empty vector,the BC group was given the conventional common medium without other treatment.Then using RT-PCR method and Westren blotting method to assay the expression of NR4A1 mRNA and protein after transfection.Results: The cDNA of NR4A1 was cloned,and its recombinant eukaryotic expression vector was constructed successfully.After the transfection,the level of expression of NR4A1 mRNA and protein was significantly higher than the level of the BC group(P<0.05) and NC group(P<0.05),while there was no significantly difference between the two groups(P>0.05).Conclusion: Through gene recombination technology,the pIERS2-ZsGreen1-NR4A1 expression vector is successfully constructed and effective expressed in H9C2 cardiomyocytes,which can further explore the biological function and mechanism of the NR4A1 gene in cardiomyocytes apoptosis.

With the improvement of living standards,the incidence rate of coronary heart disease was increased in recent years.To a large extent,the regenerated blood vessels improve the blood supply of myocardium.Whether it was in vivo or in vitro,the most research about proangiogenic cytokine which induce the angiogenesis used the single angiogenic factor to date.The curative effect was limited.In recent years,the study about gene therapy of angiogenesis showed a new method for ischemic heart disease.As the development of genetic engineering,the evolution of the technology of gene recombination and gene chip offered a good basis for the study of angiogenesis at the gene level.Now this review is talking about the gene therapy of angiogenesis.