ABSTRACT
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.