Research progress of long noncoding RNAs regulating human chondrocyte inflammatory signaling pathways in osteoarthritis / 中国药理学通报

Osteoarthritis is the commonest joint disease, but its etiology is still not clear.Recently the role of inflammation in its pathogenesis has been attached increasingly importance.Long noncoding RNAs (LncRNAs) play a key role in regulating the occurrence and development of inflammation-related diseases.This artiele reviews the research progress of LncRNAs in regula ting the occurrence and development of osteoarthritis through various endochondral inflammation signaling pathways in recent years , exploring the application of LncRNAs as a potential therapeutic target in the prevention and treatment of osteoarthritis.

Effects of miR-29b-3p targeting PTEN on congenital heart disease / 西安交通大学学报(医学版)

【Objective】 To investigate the effects of miR-29b-3p on congenital heart disease and its mechanism. 【Methods】 The expression level of miR-29b-3p in serum from CHD patients and normal individuals， and in cells was detected by RT-qPCR. Dimethylsulfoxide （DMSO） was used to induce P19 cells to differentiate into cardiomyocytes. Western blot was used to measure the expression levels of cardiogenesis-associated genes， and phosphatase and tensin homolog （PTEN） level in cells. The proliferation and migration of cardiomyocytes were measured by CCK-8 and Transwell assay， respectively. Dual-luciferase gene reporter assay was used to verify the targeted relationship between miR-29b-3p and PTEN. 【Results】 Compared with that of normal individuals， the expression of miR-29b-3p in CHD patients was decreased. During differentiation， miR-29b-3p level was higher at late stage than that at early stage. Downregulated miR-29b-3p inhibited the differentiation of P19 cells into cardiomyocytes， and inhibited cell proliferation and migration. miR-29b-3p targeted PTEN. The increased PTEN level induced by miR-29b-3p knockdown inhibited the differentiation of P19 cells， and proliferation and migration of cardiomyocytes. 【Conclusion】 miR-29b-3p was downregulated in the serum of CHD patients. The downregulation of miR-29b-3p inhibited the differentiation of P19 cells， proliferation and migration of cardiomyocytes by targeting and regulating PTEN.

Targeted regulation of SHOX2 gene expression by miR-375 in human esophageal squamous cancer cells / 医学研究生学报

Objective MiR-375 is lowly expressed in esophageal squamous cancer cells and the downstream target gene of miR-375 remains unclear .This paper discusses the role of miR-375 in regulating the expression of short stature homobox 2 ( SHOX2) in human esophageal squamous cancer cells . Methods The bioinformatics software TargetScan , miRanda, PicTar, miRTarget2, and PITA were used to predict the assumptive targets of miR-375 in SHOX2.Then, two recombinant luciferase gene report plasmids containing wild pSHOX2 3′UTR ( pSHOX2-375-WT ) and mutant pSHOX2 3′UTR ( pSHOX2-375-mut ) were constructed , sequenced , and identified.Human esophageal squamous cancer cells were co-transfected with miR-375 mimics and pSHOX2-375-WT or pSHOX2-375-mut, respectively , and divided into 7 groups: pmiR, pSHOX2-375-WT, pSHOX2-375-WT +miR-375, pSHOX2-375-WT +miR-NC, pSHOX2-375-mut, pSHOX2-375-mut+miR-375, and pSHOX2-375-mut+miR-NC, each subjected to the measurement of luciferase activity .The expressions of SHOX 2 mRNA and protein were de-termined after transfection of the esophageal squamous cancer cells with miR-375 mimics, and so were the expressions of miR-375 and SHOX2 in the esophageal squamous carcinoma tissue samples obtained postoperatively . Results Prediction with the five software showed only one conserved function site of miR-375 in SHOX2 3′UTR at 1156-1170 bp.Luciferase activity was significantly lower in the pSHOX2-375-WT+miR-375 group (0.261 ±0.036) than in the pmiR (1.818 ±0.061), pSHOX2-375-WT (1.820 ±0.086), pSHOX2-375-WT+miR-NC (1.851 ±0.094), pSHOX2-375-mut (1.861 ±0.059), pSHOX2-375-mut +miR-375 (1.896 ± 0.048), and pSHOX2-375-mut+miR-NC group (1.760 ±0.062) ( P<0.01).SHOX2 mRNA and protein expressions were sup-pressed by the overexpression of miR-375 in the EC9706 cells.The expression of miR-375 was decreased, while that of SHOX2 in-creased in the esophageal squamous carcinoma tissue as compared with the normal esophageal tissue . Conclusion MiR-375 regu-lates the expression of the SHOX 2 gen in esophageal squamous cancer cells .

Target regulation of miR-9 to the expression of NRP1 and its role in radiation effects / 中华放射医学与防护杂志

Objective To explore the effect of miR-9 on the expression of NRP1 and its radiation effects in A549 cells.Methods Bioinformatics was used to analyze the potential binding sites of has-miR-9 and NRP1-3'UTR.The miR-9 sequence was inserted into pcDNA-DEST-47 plasmid to construct the eukaryotic expression vector (pcDNA-DEST-miR-9) and to construct the NRP1 gene 3'UTR luciferase reporter plasmid (pEZX-MT05) at the same time.They were simultaneously transferred into A549 cells for analysis of the regulatory effect of miR-9 on the expression of NRP1.Meanwhile miR-29b was used as a negative control to observe whether or not NRP1 gene was a target of miR-9.After 10 Gy irradiation,the expression of NRP1,and the inhibitory effect of miR-9 on it was confirmed by Western blot assay.The expression of miR-9 was detected by real-time PCR.Results It was found that miR-9 reduced the luciferase activity of NRP1-3'UTR wild plasmid (t =3.906,P ＜ 0.05) but not NRP1-3' UTR mutant plasmid.This luciferase activity was not inhibited by other types of miRNA (miR-29b).The expression of NRP1 protein in A549 cells was decreased after the cells were transfected with miR-9 mimic.After irradiation with dose of 10 Gy,the expression of miR-9 were decreased (t =37.319,P ＜ 0.05) and the expression of NRP1 protein were increased.Conclusions miR-9 regulates the expression of NRP1 by targeting 3'UTR site of NRP1 gene in A549 cells.