首页> 外文期刊>American Journal of Physiology >Alteration in expression of myosin isoforms in detrusor smooth muscle following bladder outlet obstruction.
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Alteration in expression of myosin isoforms in detrusor smooth muscle following bladder outlet obstruction.

机译:膀胱出口梗阻后逼尿肌平滑肌中肌球蛋白同工型的表达变化。

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摘要

Partial urinary bladder outlet obstruction (PBOO) in men, secondary to benign prostatic hyperplasia, induces detrusor smooth muscle (DSM) hypertrophy. However, despite DSM hypertrophy, some bladders become severely dysfunctional (decompensated). Using a rabbit model of PBOO, we found that although DSM from sham-operated bladders expressed nearly 100% of both the smooth muscle myosin heavy chain isoform SM-B and essential light chain isoform LC17a, DSM from severely dysfunctional bladders expressed as much as 75% SM-A and 40% LC17b (both associated with decreased maximum velocity of shortening). DSM from dysfunctional bladder also exhibited tonic-type contractions, characterized by slow force generation and high force maintenance. Immunofluorescence microscopy showed that decreased SM-B expression in dysfunctional bladders was not due to generation of a new cell population lacking SM-B. Metabolic cage monitoring revealed decreased void volume and increased voiding frequency correlated with overexpression of SM-A and LC17b. Myosin isoform expression and bladder function returned toward normal upon removal of the obstruction, indicating that the levels of expression of these isoforms are markers of the PBOO-induced dysfunctional bladders.
机译:继发于良性前列腺增生的男性部分膀胱出口梗阻(PBOO)诱发逼尿肌平滑肌(DSM)肥大。但是,尽管DSM肥大,但某些膀胱仍严重功能失调(失代偿)。使用PBOO的兔模型,我们发现,尽管假手术膀胱的DSM表达了平滑肌肌球蛋白重链亚型SM-B和必需轻链异构体LC17a的近100%,但严重功能异常的膀胱的DSM却表达了多达75% %SM-A和40%LC17b(均与最大起酥油速度降低有关)。膀胱功能障碍的DSM还表现出强直型收缩,其特征是产生力缓慢且维持力高。免疫荧光显微镜检查显示,功能障碍性膀胱中​​SM-B表达的降低并不是由于缺少SM-B的新细胞群的产生。代谢笼监测显示,与SM-A和LC17b的过表达相关的空隙体积减少和空隙频率增加。去除梗阻后,肌球蛋白同工型表达和膀胱功能恢复正常,表明这些同工型的表达水平是PBOO诱导的功能障碍性膀胱的标志物。

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