Wang Z E, Gopalakurup S K, Levin R M, Chacko S
Department of Pathobiology, University of Pennsylvania, Philadelphia, USA.
Lab Invest. 1995 Aug;73(2):244-51.
Partial ligation of the urinary out-flow tract of rabbit bladder induces hypertrophy of the smooth muscle layer in the bladder wall, and it is reversible by the removal of the ligature. The expression of smooth muscle myosin heavy chain isoforms SM1 and SM2 after hypertrophy and the regression of hypertrophy (reversal) was investigated at the translational and transcriptional levels using this experimental model.
The contractile activity of smooth muscle strips derived from normal, hypertrophied, and reversal bladders was measured using electrical stimulation. Expression of SM1 and SM2 in normal, hypertrophied, and reversal muscle tissue was characterized using SDS-PAGE, reverse transcriptase-PCR (RT-PCR), and RNase protection assay.
Smooth muscle strips from hypertrophied urinary bladder revealed a decrease in both force and rate of force generation in response to field stimulation. These alterations in contractility were reversed by removal of the obstruction. The altered function in bladder hypertrophy was also associated with changes in translation and transcription of the smooth muscle heavy chain isoforms SM1 and SM2. Upon regression of the hypertrophy by removal of the obstruction, the relative ratio of myosin heavy chain SM2:SM1 returned to nearly normal values. Analyses by RT-PCR showed a decrease in the mRNA transcript for SM2 in hypertrophied bladder muscle; and, on reversal of the hypertrophy, the SM2 mRNA level returned to that of normal bladder. These data suggest that the obstruction-induced hypertrophy activates a down-regulating mechanism for the expression of myosin SM2 heavy chain.
Obstruction-induced alteration in the contractile characteristics of the urinary bladder smooth muscle is associated with changes in the expression of smooth muscle myosin heavy chains at both the protein and mRNA levels. The contractile function and the myosin heavy chain expression return to normal after regression of the smooth muscle hypertrophy on removal of the obstruction.
兔膀胱尿路部分结扎可导致膀胱壁平滑肌层肥大，去除结扎后肥大是可逆的。利用该实验模型，在翻译和转录水平研究了肥大及肥大消退（逆转）后平滑肌肌球蛋白重链亚型SM1和SM2的表达。
使用电刺激测量来自正常、肥大和逆转膀胱的平滑肌条的收缩活性。使用SDS-PAGE、逆转录聚合酶链反应（RT-PCR）和核糖核酸酶保护分析来表征正常、肥大和逆转肌肉组织中SM1和SM2的表达。
肥大膀胱的平滑肌条在电场刺激下显示出力量和力量产生速率的降低。去除梗阻后，这些收缩性改变得以逆转。膀胱肥大中功能的改变也与平滑肌重链亚型SM1和SM2的翻译和转录变化有关。通过去除梗阻使肥大消退后，肌球蛋白重链SM2:SM1的相对比例恢复到接近正常的值。RT-PCR分析显示，肥大膀胱肌肉中SM2的mRNA转录物减少；肥大逆转后，SM2 mRNA水平恢复到正常膀胱水平。这些数据表明，梗阻诱导的肥大激活了肌球蛋白SM2重链表达的下调机制。
梗阻诱导的膀胱平滑肌收缩特性改变与平滑肌肌球蛋白重链在蛋白质和mRNA水平的表达变化有关。去除梗阻后平滑肌肥大消退，收缩功能和肌球蛋白重链表达恢复正常。
