Degradation of submandibular gland AQP5 by parasympathetic denervation of chorda tympani and its recovery by cevimeline, an M3 muscarinic receptor agonist.

Degradation of submandibular gland AQP5 by parasympathetic denervation of chorda tympani and its recovery by cevimeline, an M3 muscarinic receptor agonist.
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DOI:
10.1152/ajpgi.00359.2007
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发表时间:
2008-07
期刊:
American journal of physiology. Gastrointestinal and liver physiology
影响因子:
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通讯作者:
Xuefei Li;A. Azlina;M. Karabasil;N. Purwanti;T. Hasegawa;C. Yao;T. Akamatsu;K. Hosoi
Xuefei Li;A. Azlina;M. Karabasil;N. Purwanti;T. Hasegawa;C. Yao;T. Akamatsu;K. Hosoi
中科院分区:
其他
文献类型:
--
作者:
Xuefei Li;A. Azlina;M. Karabasil;N. Purwanti;T. Hasegawa;C. Yao;T. Akamatsu;K. Hosoi

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通过鼓索去神经(CTD,副交感神经切除术),水通道蛋白5(AQP 5),而不是AQP 1,蛋白水平在大鼠下颌下腺(SMG)中显著降低,在4周时下降到对侧腺体的37%。AQP 5和AQP 1的蛋白水平没有显着影响颈交感神经干(交感神经切除术)去神经支配。给予盐酸西维美林(一种M3毒蕈碱受体激动剂)(10 mg/kg,po 7天),但不给予毛果芸香碱(0.3 mg/kg,po 7天),可恢复CTD降低的AQP 5蛋白水平,并使AQP 1蛋白水平高于对照水平。CTD和盐酸西维美林给药对AQP 5 mRNA水平几乎没有影响。氯喹(50 mg/kg,连续7天,po),一种溶酶体变性剂,增加了CTD降低的AQP 5蛋白水平。从下颌下溶酶体组分中获得的提取物在体外降解总膜组分中的AQP 5蛋白。这些结果表明,可能的调节AQP 5蛋白水平的SMG的副交感神经/M3毒蕈碱受体激动剂,并意味着参与溶酶体酶,但不是一个转录机制,在这种调节。
By chorda tympani denervation (CTD, parasympathectomy), the aquaporin 5 (AQP5), but not AQP1, protein level in the rat submandibular gland (SMG) was significantly decreased, dropping to 37% of that of the contralateral gland at 4 wk. The protein levels of AQP5 and AQP1 were not significantly affected by denervation of the cervical sympathetic trunk (sympathectomy). Administration of cevimeline hydrochloride, an M3 muscarinic receptor agonist (10 mg/kg for 7 days po), but not pilocarpine (0.3 mg/kg for 7 days po), recovered the AQP5 protein level reduced by CTD and increased the AQP1 protein level above the control one. The mRNA level of AQP5 was scarcely affected by CTD and cevimeline hydrochloride administration. Administration of chloroquine (50 mg/kg for 7 days po), a denaturant of lysosomes, increased the AQP5 protein level reduced by CTD. An extract obtained from the submandibular lysosomal fraction degraded the AQP5 protein in the total membrane fraction in vitro. These results suggest the possible regulation of the AQP5 protein level in the SMG by the parasympathetic nerves/M3 muscarinic receptor agonist and imply the involvement of lysosomal enzymes, but not a transcriptional mechanism, in this regulation.