摘要或動機

高血壓所誘發的機械性展延是造成心肌肥大的基本因子，本實驗即藉由微陣列基因分析法同時大量的分析機械性展延所造成心肌細胞的基因表現。將新生鼠的心肌細胞施以 20﹪的機械性展延，抽取其 mRNA製作成 cDNA 探針與現成的 cDNA 晶片進行雜漬反應 （此晶片上包含了 480個如訊息傳遞、控制細胞生長週期、細胞骨架等的已知基因），在眾多有因為機械性展延而造成基因表現差異的基因中，我們選擇了 eNOS 基因（內皮細胞 NO合成?）進行西方墨點法及 NOS活性和 NO 產生量測定的實驗，進一步證實 eNOS 的基因表現量的確是增加的，此一結果與微陣列基因分析所得之結果不謀而合。 Mechanical stretch induced by high blood pressure is an initial factor laeding to cardiac\r
hypertrophy. The use of cDNA microarrays has made it possible to simultaneously analyze\r
stretch-induced gene expression in cardiomyocytes. Neonatal rat cardiomyocytes were cultured on\r
malleable silicone dishes and were stretched by 20%. We compared the transcript profiles of\r
cardiomyocytes under mechanical stretch for 60 minutes by hybridization of cell-derived cDNA to\r
DNA probes immobilized on microarrays. The microarrays contained probes for 480 known genes\r
including signal transduction, cell cycle regulators, cytoskeleton and cell motility, and so on. Eighteen\r
genes were indentified that showed significantly differential expression in response to mechanical\r
stretch in cardiomyocytes. Of the represented genes expressed, endothelial nitric oxide synthase (eNOS)\r
genes was the most interesting one. Northern blot and western blot analysis further quantified the\r
expression of eNOS gene. Mechanical stretch also increased constitutive NOS activity and NO\r
production. Our results indicate that mechanical stretch induces eNOS gene expression thus increases\r
constitutive NOS activity and NO production in cardiomyocytes.