Effect of lncRNA MALAT1 on myocardial infarction mice by regulation of miR-200a-3p targeting BTG2 axis
XING Xiaowei
SUN Jianhua
YANG Yang
XUAN Huihong
FU Binbin
DONG Shuang
Abstract：Objective To investigate the effect of long non-coding RNA(lncRNA)metastasis-associated lung adenocarcinoma transcript 1(MALAT1)on cardiomyocyte apoptosis in acute myocardial infarction(AMI)mice by regulating the microRNA-200a-3p(miR-200a-3p)/B-cell translocation gene 2(BTG2)axis.Methods A total of 108 SPF C57BL/6J male mice were subjected,and 18 of them were randomly assigned into a control group.Then a mouse model of AMI was established in the remaining 90 mice,which were further divided into Model group,Silence control group(sh-NC group),Silencing MALAT1 group(sh-MALAT1 group),Silencing MALAT1+inhibition control group(sh-MALAT1+anti-NC group),and Silencing MALAT1+inhibited miR-200a-3p group(sh-MALAT1+anti-miR-200a-3p group),with 18 mice in each group.Mouse heart function and the expression of lncRNA MALAT1,miR-200a-3p,and BTG2 in myocardial tissues were detected,and the myocardial infarction area mice was measured.Pathological changes in myocardial tissues were observed.Cardiomyocyte apoptosis and expression of apoptosis-related proteins were detected.Results Compared with the Control group,the Model group exhibited significantly decreased left ventricle ejection fraction(LVEF),obviously increased left ventricular end-diastolic diameter(LVEDD),left ventricular end-systolic diameter(LVESD)and apoptotic rate,larger myocardial infarction area,up-regulated levels of lncRNA MALAT1,BTG2,Bax and Caspase-3,and down-regulated miR-200a-3p expression(P<0.05).Silencing MALAT1 resulted in increased LVEF[(46.79±4.83)%vs(62.47±6.48)%],and reduced LVEDD(5.16±0.53 mm vs 3.28±0.37 mm),LVESD(7.28±0.74 mm vs 6.01±0.61 mm),decreased myocardial infarction area[(15.69±2.75)%vs(29.78±4.38)%],down-regulated lncRNA MALAT1(0.58±0.06 vs 1.70±0.07),BTG2(0.54±0.05 vs 1.43±0.14),Bax(0.56±0.05 vs 0.94±0.09)and Caspase-3(0.62±0.06 vs 1.03±0.11),and upregulated miR-200a-3p(1.51±0.15 vs 0.55±0.05)when compared with the sh-NC group(P<0.05).The sh-MALAT1+anti-miR-200a-3p group had significantly reduced LVEF,increased LVEDD,LVESD and apoptotic rate,enlarged myocardial infarction area,up-regulated expression of BTG2,Bax,and Caspase-3,and down-regulated expression of miR-200a-3p than the Silensing MALAT1+inhibition control group(P<0.05).Conclusion Inhibition of lncRNA MALAT1 expression suppresses cardiomyocyte apoptosis in AMI mice by targeting the miR-200a-3p/BTG2 axis.
Keywords：myocardial infarctionmicroRNAsB-cell translocation gene 2-axismetastasis-associated lung adenocarcinoma transcript 1
Publication Date：2026-01-15
Online Publishing Date：2026-01-16(First online date of this platform, not the publication date of the document)
Pages：6( 107-112 )