Background:microRNAs are crucial for cardiovascular development and are associated with congenital heart disease(CHD).Recent studies have shown that microRNAs play a role in heart development and is closely related to...Background:microRNAs are crucial for cardiovascular development and are associated with congenital heart disease(CHD).Recent studies have shown that microRNAs play a role in heart development and is closely related to CHD.The present study investigated the underlying mechanism of microRNA-208a(miR-208a)in“simple”CHD.Material and Methods:Reverse transcription-quantitative PCR(RT-qPCR)demonstrated miR-208a expression levels in children with CHD(n=27)compared with normal controls(n=29),in cardiomyocytes from embryo 10(E10)to post-birth(P7)and organs in adult rats in healthy rats.Apoptosis of H9c2 cells after transfection with miR-208a detected by TUNEL assay.B-cell lymphoma(Bcl)-2,an anti-apoptotic gene,was detected by RT-qPCR,as well as Gata4.After 48h overexpression of miR-208a,GATA4 was detected via western blotting.Dual luciferase reporting system was used to identify the binding sites of miR-208a to Gata4.Results:Expression of miR-208a was upregulated in the CHD group via the control group(p<0.01).At P7,miR-208a had the highest expression(p<0.01),and which was highest in myocardiocytes via other organs or tissues(p<0.01)in adult rats.The number of apoptotic cells increased significantly post-transfection with miR-208a(p<0.01),while decreased with the miR-208a inhibitor via the control group(p<0.01).Compared with the control group,there was no significant difference in the expression level of Bcl-2 after miR-208a overexpression(p>0.05).The present study proved that miR-208a binds directly to the 3´-UTR of Gata4 at site 1,363-1,369 bp.Expression of GATA4 decreased after miR-208a overexpression(p<0.01),but increased following transfection with a miR-208a inhibitor via the control group(p<0.05).Conclusions:Our study demonstrated that miR-208a downregulates Bcl-2 by directly targeting GATA4,which may cause CHD.miR-208a may become a new biomarker or therapeutic target for CHD in the future.展开更多
Balanoposthitis(BP),a common male genitalia inflammation,is managed by clinicians from different specialties,including urology,pediatrics,dermatology,and venereology.Due to this diverse array of clinicians involved,th...Balanoposthitis(BP),a common male genitalia inflammation,is managed by clinicians from different specialties,including urology,pediatrics,dermatology,and venereology.Due to this diverse array of clinicians involved,there exists a lack of consistent,evidence-based recommendations for BP.The development of the consensus engaged 19 representative hospitals and it adhered to rigorous protocols,encompassing international registration(IPGRP-2021CN003)and the application of evidence grading criteria and recommendation standards[Appendix S1,Supplementary File,http://links.lww.com/CM9/C42].Over the period from December 2020 to October 2022,consensus on 12 clinical issues was reached through comprehensive evidence searches and two iterations of Delphi surveys[Supplementary File,http://links.lww.com/CM9/C42].展开更多
基金The work was supported by the National Science Foundation of China(No.8170131).
文摘Background:microRNAs are crucial for cardiovascular development and are associated with congenital heart disease(CHD).Recent studies have shown that microRNAs play a role in heart development and is closely related to CHD.The present study investigated the underlying mechanism of microRNA-208a(miR-208a)in“simple”CHD.Material and Methods:Reverse transcription-quantitative PCR(RT-qPCR)demonstrated miR-208a expression levels in children with CHD(n=27)compared with normal controls(n=29),in cardiomyocytes from embryo 10(E10)to post-birth(P7)and organs in adult rats in healthy rats.Apoptosis of H9c2 cells after transfection with miR-208a detected by TUNEL assay.B-cell lymphoma(Bcl)-2,an anti-apoptotic gene,was detected by RT-qPCR,as well as Gata4.After 48h overexpression of miR-208a,GATA4 was detected via western blotting.Dual luciferase reporting system was used to identify the binding sites of miR-208a to Gata4.Results:Expression of miR-208a was upregulated in the CHD group via the control group(p<0.01).At P7,miR-208a had the highest expression(p<0.01),and which was highest in myocardiocytes via other organs or tissues(p<0.01)in adult rats.The number of apoptotic cells increased significantly post-transfection with miR-208a(p<0.01),while decreased with the miR-208a inhibitor via the control group(p<0.01).Compared with the control group,there was no significant difference in the expression level of Bcl-2 after miR-208a overexpression(p>0.05).The present study proved that miR-208a binds directly to the 3´-UTR of Gata4 at site 1,363-1,369 bp.Expression of GATA4 decreased after miR-208a overexpression(p<0.01),but increased following transfection with a miR-208a inhibitor via the control group(p<0.05).Conclusions:Our study demonstrated that miR-208a downregulates Bcl-2 by directly targeting GATA4,which may cause CHD.miR-208a may become a new biomarker or therapeutic target for CHD in the future.
基金National Natural Science Foundation of China(No.82273538)Public Health Research and Development Program of the Shenyang Science and Technology Bureau(No.22-321-33-12)National Key R&D Program of China(No.2023YFC2508200)
文摘Balanoposthitis(BP),a common male genitalia inflammation,is managed by clinicians from different specialties,including urology,pediatrics,dermatology,and venereology.Due to this diverse array of clinicians involved,there exists a lack of consistent,evidence-based recommendations for BP.The development of the consensus engaged 19 representative hospitals and it adhered to rigorous protocols,encompassing international registration(IPGRP-2021CN003)and the application of evidence grading criteria and recommendation standards[Appendix S1,Supplementary File,http://links.lww.com/CM9/C42].Over the period from December 2020 to October 2022,consensus on 12 clinical issues was reached through comprehensive evidence searches and two iterations of Delphi surveys[Supplementary File,http://links.lww.com/CM9/C42].