CAJ | 학술논문

目的:应用基因微阵列研究分析风湿性心脏病所致心力衰竭(风心病心衰)患者以及正常成人的左心室心肌基因表达谱,筛选出风心病心衰相关靶基因.方法:采用6张人类全基因组微阵列HG U133 Plus 2.0 GeneChip,分别构建风心病心衰患者(实验组n=15)与正常对照组(n=9)的左心室乳头肌基因表达谱.运用GeneSpring软件筛选出两组间差异表达基因,作为风心病心衰相关靶基因,并进行生物信息学分析.采用实时荧光定量多聚酶链反应(Real-time PCR),对其中3个靶基因进行验证.结果:确定102个风心病心衰相关靶基因,并将它们归入7个风心病心衰相关基因群.实时荧光定量多聚酶链反应检测证实,风心病心衰患者左心室心肌内,基因NPPB与IGFBP2明显上调,ATF3明显下调,与基因微阵列实验结果非常吻合,说明基因微阵列实验结果可靠.结论:风心病心衰发生发展过程中存在众多基因表达的改变,全基因组表达谱的研究有助于认识该综合征的发病机制.对风心病心衰相关靶基因的深入研究,有助于揭示该综合征发病学上的遗传标志以及分子机制.
목적:응용기인미진렬연구분석풍습성심장병소치심력쇠갈(풍심병심쇠)환자이급정상성인적좌심실심기기인표체보,사선출풍심병심쇠상관파기인.방법:채용6장인류전기인조미진렬HG U133 Plus 2.0 GeneChip,분별구건풍심병심쇠환자(실험조n=15)여정상대조조(n=9)적좌심실유두기기인표체보.운용GeneSpring연건사선출량조간차이표체기인,작위풍심병심쇠상관파기인,병진행생물신식학분석.채용실시형광정량다취매련반응(Real-time PCR),대기중3개파기인진행험증.결과:학정102개풍심병심쇠상관파기인,병장타문귀입7개풍심병심쇠상관기인군.실시형광정량다취매련반응검측증실,풍심병심쇠환자좌심실심기내,기인NPPB여IGFBP2명현상조,ATF3명현하조,여기인미진렬실험결과비상문합,설명기인미진렬실험결과가고.결론:풍심병심쇠발생발전과정중존재음다기인표체적개변,전기인조표체보적연구유조우인식해종합정적발병궤제.대풍심병심쇠상관파기인적심입연구,유조우게시해종합정발병학상적유전표지이급분자궤제.
Objective:To analyze gene expression profiling of left ventricular myocardium in patients with chronic congestive heart failure(CHF)caused by rheumatic heart disease(RHD)with the normal controls in order to identify CHF associated target genes. Methods:The gene expression profiles of left ventricular myocardium from patients with CHF by RHD and normal controls were obtained from six human whole-genomic oligonucleotide microarrays(Affymetrix HG U133 Plus 2.0 GeneChip). GeneSpring software was used to identify the differentially expressed genes in both groups,and bioinformatic analysis was applied to analyze the target genes associated with CHF. Real-time PCR was carried out to validate the expression of three target genes. Results:We identified 102 target genes associated with CHF which were classified into 7 gene clusters. Microarray results were further confirmed by real time PCR for three genes. ATF3 was markedly down-regulated,IGFBP2 and NPPB were notably up-regulated in the left ventricular myocardium samples from CHF patients. Conclusion:A lot of differentially expressed genes,obtained by using the whole-genomic expression profiling technology,might be a contributory factor for the initiation and progression of CHF and it helpful for the understanding of underlying pathophysiological implications. Further investigation on these genes would provide a strategy to identify genetic markers and molecular events associated with CHF caused by RHD.