The assessment of the contractility of the proliferating vascular smooth muscle

本研究的目的是探讨增殖的气道平滑肌收缩的机制。通过插入巨细胞病毒启动子和目的基因，构建了高效感染哺乳动物细胞的重组杆状病毒载体。该病毒可成功地转染NIH3T3成纤维细胞、猪气管平滑肌细胞和猪冠状动脉平滑肌细胞。我们花了很长时间来优化转染法的条件。然而，我们可以通过改进重组杆状病毒的纯化工艺来克服这一问题。2.我们还可以通过将培养的平滑肌细胞重组为组织样制剂来建立测量等长张力的方法。RhoA转基因细胞的收缩能力是对照组的2-3倍。3.相反，RNA干扰下调RhoA的表达大大抑制了血管的收缩。

The purpose of the present study was to investigate the mechanism underlying the contractility of the proliferating airway smooth muscle. We could obtain the following results.1, Wd could construct the recombinant baculo virus vector, which can be infected with a high efficiency to the mammalian cell, by inserting the cytomegalo virus promoter and the cDNA of interest. This virus could successfully transfected to the NIH 3T3 fibroblast, porcine tracheal smooth muscle cells and porcine coronary smooth muscle cells. It took us long time to optimize the condition for the transfection. However, we could overcome this problem by modifying the purification process of the recombinant baculo virus.2, We could also establish the method to measure isometric tension using the cultured smooth muscle cells by reconstituting these cells into tissue-like preparation. The RhoA transfected cells showed 2-3 times greater contractility, compared with the control treatment.3, On the contrary, the knock-down of RhoA expression by RNA interference greatly inhibited the smooth muscle contractility.