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首页> 外文期刊>American Journal of Physiology >BDNF overexpression in the bladder induces neuronal changes to mediate bladder overactivity
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BDNF overexpression in the bladder induces neuronal changes to mediate bladder overactivity

机译：BDNF在膀胱中过表达诱导神经元变化以介导膀胱过度

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摘要

Elevated levels of brain-derived neurotrophic factor (BDNF) in urine of overactive bladder (OAB) patients support the association of BDNF with OAB symptoms, but the causality is not known. Here, we investigated the functionality of BDNF overexpression in rat bladder following bladder wall transfec-tion of either BDNF or luciferase (luciferase) transgenes (10 μg). One week after transfection, BDNF overexpression in bladder tissue and elevation of urine BDNF levels were observed together with increased transcript of BDNF, its cognate receptors (TrkB and p75~(NTR)), and downstream PLCγ isoforms in bladder. BDNF overexpression can induce the bladder overactivity (BO) phenotype which is demonstrated by the increased voiding pressure and reduced intercontractile interval during transurethral open cystometry under urethane anesthesia. A role for BDNF-mediated enhancement of prejunctional cholin-ergic transmission in BO is supported by the significant increase in the atropine- and neostigmine-sensitive component of nerve-evoked contractions and upregulation of choline acetyltransferase, vesicular ace-tylcholine transporter, and transporter Oct2 and -α1 receptors. In addition, higher expression of transient receptor channels (TRPV1 and TRPA1) and pannexin-1 channels in conjunction with elevation of ATP and neurotrophins in bladder and also in L6/S1 dorsal root ganglia together support a role for sensitized afferent nerve terminals in BO. Overall, genomic changes in efferent and afferent neurons of bladder induced by the overexpression of BDNF per se establish a mechanistic link between elevated BDNF levels in urine and dysfunctional voiding observed in animal models and in OAB patients.
机译：过度活性膀胱（OAB）患者尿液中脑衍生的神经营养因子（BDNF）的升高水平支持BDNF与OAB症状的关联，但不知道的因果关系。在此，我们研究了在BDNF或荧光素酶（Luciferase）转基因（10μg）的膀胱壁转移后大鼠膀胱中BDNF过表达的功能。转染后一周后，将膀胱组织中的BDNF过表达和尿液BDNF水平的升高与BDNF的增加的转录物，其同源受体（TRKB和P75〜（NTR））和膀胱下的下游PLCγ同种型。 BDNF过表达可以诱导膀胱过度屈服（BO）表型，其通过增加的空隙压力和在氨基甲酸酯麻醉下在经尿性开放囊体中的转移间隔减少的间隔。通过诱发神经诱发收缩和胆碱乙酰转移酶，囊泡ACE-甲胆碱转运蛋白，尿道α-葡萄酒转运蛋白和转运蛋白的上调性的阿托嘌呤和Neostigmine敏感成分的显着增加，支持BDNF介导的预期胆碱 - ERGIC传播的作用。和-α1受体。此外，瞬时受体通道（TRPV1和TRPA1）和Pannexin-1的表达结合在膀胱中的ATP和神经营养素的升高以及L6 / S1背根神经节的升高结合在一起，将敏感的传入神经终端在博中的作用。总体而言，由BDNF的过表达诱导的BDNF本身诱导的膀胱传育和传入神经元的基因组变化在动物模型和OAB患者中观察到尿液和功能障碍尿液中升高的BDNF水平之间的机械联系。

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