Molecular basis of the formation of endolymphatic hydrops in Meniere's disease

为了确定梅尼埃病中内淋巴水肿形成的分子机制，我们采用RT-PCR（逆转录聚合酶链反应）、DNA测序、原位杂交和免疫组织化学等分子生物学技术检测了大鼠内耳中几种受体和通道的表达。内皮素受体、矿化皮质激素I型受体、β -肾上腺素能受体和水通道的表达。腺苷酸环化酶环AMP系统可能通过调节Cl离子在淋巴内间隙和淋巴周围间隙之间的运输而导致急性淋巴内水肿。水通道，AQP2和AQP3也可能是内淋巴水肿形成的关键因素，因为这些高度透水的分子存在于内淋巴囊的管腔中，内淋巴被认为是相对快速吸收的。

To determine the molecular mechanism underlying the formation of endolymphatic hydrops in Meniere's desease, the expressions of several receptors and channels in the rat inner ear were examined by using molecular biological techniques including RT-PCR (reverse transcription-polymerase chain reaction), DNA sequencing, in-situ hybridization, and immunohistochemistry. The expressions of endothelin receptor, mineralocorticoid type I receptor, beta-adrenergic receptor, and water channels were identified. Adenylate cyclase-cyclic AMP system should be responsible for the acute endolymphatic hydrops by modulating the transport of Cl ion between the endolymphatic and perilymphatic spaces. Water channels, AQP2 and AQP3 may also be critical factors in the development of endolymphatic hydrops, because these highly water-permeable molecules are present in the lumen of the endolymphatic sac, where endolymph is believed to be absorbed relative rapidly.