Correlation Analysis between Serum miR-133a-3p and PTPN22 Levels Expression and Disease Severity in Patients with Psoriasis Vulgaris / 现代检验医学杂志

Objective To explore the correlation between the serum levels expression of microRNA(miR)-133a-3p,protein tyrosine phosphatase nonreceptor type 22(PTPN22)and the severity of psoriasis vulgaris.Methods A total of 86 patients with psoriasis vulgaris who were admitted to Cangzhou People's Hospital from January 2022 to June 2022 were collected as the observation group.They were separated into a progressive group(n=41)and a quiescent group(n=45)based on the area and severity of the skin lesions.Meantime,86 healthy individuals undergoing plastic surgery examinations were regarded as the control group.Real time fluorescent quantitative PCR(qRT-PCR)method was applied to detect the relative expression levels of miR-133a-3p and PTPN22 in serum.Target Scan Human website was applied to predict the targeting relationship between PTPN22 and miR-133a-3p.Spearman method was applied to analyze the correlation between the expression levels of miR-133a-3p and PTPN22 in serum of patients with psoriasis vulgaris,the psoriasis area and the psoriasis area and severity index score(PASI).Logistic regression was applied to analyze the influencing factors of severity in patients with psoriasis vulgaris.Results Compared with the control group,the serum miR-133a-3p(1.85±0.46 vs 1.05±0.21)expression level in the observation group was increased,while the PTPN22 mRNA(0.76±0.13 vs 1.02±0.18)expression level was reduced,and the difference were statistically significant(t=14.671,10.859,all P<0.05).Compared with the quiescent group,the serum miR-133a-3p(2.05±0.52 vs 1.67±0.41)expression level in the progressive group was increased,while the PTPN22 mRNA(0.66±0.11 vs 0.85±0.15)expression level was reduced and the differences were statistically significant(t=3.780,6.643,all P<0.05).Target Scan Human website predicted that there may be a targeting relationship between miR-133a-3p and PTPN22.Spearman analysis showed that there was a positive correlation between serum miR-133a-3p and PASI score in patients with psoriasis vulgaris(r=0.469,P<0.05),while serum TPN22 mRNA level was negatively correlated with PASI score(r=0.469,P<0.05).Serum miR-133a-3p[OR(95%CI)=2.884(1.261～6.595)]was an independent risk factor for the severity of psoriasis vulgaris,while PTPN22[OR(95%CI)=0.562(0.367～0.860)]was an independent protective factor(all P<0.05).Conclusion The expression level of miR-133a-3p in serum of patients with psoriasis vulgaris was increased,while the expression level of PTPN22 was reduced.The two were closely related to the PASI score and may to some extent reflect the severity of psoriasis patients.

Effects of hydrogen sulfide (HS) on cardiac hypertrophy and miRNA-133a-mediated Ca/calcineurin/NFATc4 signal pathway in rats / 中国应用生理学杂志

OBJECTIVE@#To investigate the effects of hydrogen sulfide (HS) on the negatively regulation of cardiomyocyte hypertrophy and the relationship between the effect of HS with miRNA-133a-mediated Ca/calcineurin/NFATc4 signal pathway.@*METHODS@#Cardiomyocyte hypertrophy was induced by isoproterenol (ISO). The cell surface area was measured by image analysis system (Leica). The expression of brain natriuretic peptide(BNP), β-myosin heavy chain(β-MHC), cystathionase (CSE), miRNA-133a, calcineurin (CaN) were detected by qRT-PCR. The protein expressions of CaN、nuclear factors of activated T cells (NFATc4) were detected by Western blot. The concentration of HS in the cardiomyocyte was detected by Elisa. The concentration of intracellular calcium was measured by calcium imaging using confocal microscope. The nuclear translocation of NFATc4 was checked by immuno-fluorescence cell staining technique.@*RESULTS@#①The level of system of CSE/HS and expression of miRNA-133a were significantly reduced in cardiomyocyte hypertrophy. Pretreatment with NaHS increased the concentration of HS and the expression of miRNA-133a mRNA in cardiomyocytes, and suppressed cardiomyocyte hypertrophy. ②The concentration of intracellular calcium, the expression of CaN and nulear protein NFATc4 were significantly increased, and the nuclear translocation of NFATc4 were obviously enhanced in cardiomyocyte hypertrophy. NaHS pretreatment markedly inhibited these effects of ISO induced cardiomyocyte hypertrophy. ③Application of antagomir-133a reversed the inhibitory effects of NaHS on cardiomyocyte hypertrophy, and increased the influx of intracellular calcium, and elevated the expression of CaN and nuclear protein NFATc4, and enhanced the nuclear translocation of NFATc4.@*CONCLUSIONS@#HS can negatively regulate cardiomyocyte hypertrophy. The effects might be associated with HS increasing expression of miRNA-133a and inhibiting inactivation of Ca/calcineurin/NFATc4 signal pathway.

Ursolic acid inhibits migration and invasion of human lung cancer A549 cells by targeting miRNA-133a / 中国病理生理杂志

AIM:To investigate the effects of ursolic acid ( UA) on the migration and invasion of human lung cancer cell line A549, and to explore its mechanism .METHODS:The cell viability was detected by MTT assay .The ex-pression of miRNA-133a was detected in the A549 cells treated with UA by real-time PCR.The miRNA-133a mimics and inhibitor were transfected into the A 549 cells, and the transfection efficiency was analyzed by real-time PCR.The cell mi-gratory and invasive abilities were determined by wound healing and Transwell methods , respectively .RESULTS:The via-bility of the human lung cancer A549 cells was significantly inhibited by UA in a dose-dependent manner (P<0.05).IC50 of UA (24 h) for lung cancer A549 cells was 31.04 μmol/L.UA treatment significantly inhibited the migratory and inva-sive abilities of A549 cells in a concentration-dependent manner , accompanied by significantly elevation of miRNA-133a expression.The mimics and inhibitor of miRNA-133a significantly upregulated and downregulated the expression of miRNA -133a in the transfected A549 cells, respectively.In addition, the viability of the A549 cells was decreased extremely after tansfected with the miRNA-133a mimics (P<0.01), so did the results of the cell migration and invasion test .The A549 cells tansfected with the miRNA-133a inhibitor showed an opposite changes of the cell viability , migration and invasion . CONCLUSION:UA inhibited the viability , migration and invasion of lung cancer A 549 cells by elevating the expression of miRNA-133a.

Preliminary study on miRNA-133a-3p and hypoxia in rat cardiomyocytes / 局解手术学杂志

tonomous Prefecture,Enshi Hubei 445000,China;2.Graduate School,Guangdong Medical College,Zhanjiang Guangdong 524001,China) Objective To study the relationship of miRNA-133a-3p and hypoxia in rat cardiomyocytes,and to detect the expression of the probable target genes.Methods SD rats cardiomyocytes were cultivated,and treated in hypoxia condition(37 ℃,5%CO2 ,1%O2 )for 0 hour,4 hours,8 hours,12 hours,16 hours,20 hours and 24 hours.The miRNA-133a-3p level was detected by qRT-PCR,and its biological information and target genes were predicted by targetScan picTar and miRanda,etc.Then we carried out qRT-PCR and Western blot to detect the expression of the probable target genes.Results miRNA-133a-3p expression was much higher in 4 hours hypoxia (P =0.000),then its expression gradually declined,and stabilized after 12 hours hypoxia.Bioinformatics prediction found that TGF-β1 may be its target.The mR-NA expression of TGF-β1 was obviously higher in 4 hours hypoxia than those in 0 hour and 24 hours(P Objective To study the relationship of miRNA-133a-3p and hypoxia in rat cardiomyocytes,and to detect the expression of the probable target genes.Methods SD rats cardiomyocytes were cultivated,and treated in hypoxia condition(37 ℃,5%CO2 ,1%O2 )for 0 hour,4 hours,8 hours,12 hours,16 hours,20 hours and 24 hours.The miRNA-133a-3p level was detected by qRT-PCR,and its biological information and target genes were predicted by targetScan picTar and miRanda,etc.Then we carried out qRT-PCR and Western blot to detect the expression of the probable target genes.Results miRNA-133a-3p expression was much higher in 4 hours hypoxia (P =0.000),then its expression gradually declined,and stabilized after 12 hours hypoxia.Bioinformatics prediction found that TGF-β1 may be its target.The mR-NA expression of TGF-β1 was obviously higher in 4 hours hypoxia than those in 0 hour and 24 hours(P <0.05).And the protein expression of TGF-β1 was significantly higher in 4 hours hypoxia(P <0.05).Conclusion miRNA-133a-3p may participate in cardiomyocytes necrosis in rats through regulating TGF-β1.