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膵外分泌細胞における受容体調節

外分泌胰腺细胞的受体调节

基本信息

批准号：
63570320
负责人：
安達秀樹
金额：
$ 1.28万
依托单位：
Kyoto University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1988
资助国家：
日本
起止时间：
1988 至无数据
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-63570320/
关键词：
CCKレセプタームスカリンレセプター VIPレセプター CCK ボンベシン cGMP TPA P-Iターンオーバー

项目摘要

63年度研究課題とした1)CCK受容体調節の細胞内機構、2)ムスカリン様受容体の調節機構および3)VIP受容体の調節に関して以下の如き成績を得た。(1)CCK受容体調節の細胞内機構:既報の如くCCK受容体は、ムスカリン様受容体を介する細胞機構の活性化によって、その高親和性結合部位を失う。同様の成績はTPAによっても再現される。今回新たに、もう一つのCa依存性ホルモンであるボンベシンのCCK受容体への影響を検討したところ、ボンベシンも前二者と同様、CCK受容体の高親和性結合部位を抑制した。しかしながら、ボンベシンは、ムスカリン様受容体刺激と異なり、細胞内PーI代謝回転の産物であるDGやIPを増加させず、全く異なる未知の細胞内機構によってCCK受容体を制御していると考えられた。(2)ムスカリン様受容体の調節機構:前者と逆に、CCKはやはりムスカリン様受容体の高親和性結合部位を制御し、同様の現象はTPAによっても再現されたところから、この制御には、CCKによるPーI代謝回転及びPKーCの関与が考えられた。しかしながら、前者と異なり、ボンベシンはムスカリン様受容体に影響を与えず、ムスカリン様受容体の制御にはボンベシン受容体を通じて活性化される細胞機構は関与しないものと考えられた。(3)VIPの受容体調節:VIP受容体結合はCCKによって制御され、その本態は高親和性結合部位の消失によるものであった。この受容体制御はVIPの生物活性に直接影響し、VIPによるcAMP増加及びアミラーゼ分泌はCCK存在下では抑制された。CCKの活性化する細胞内機構の一つであるcGMPの増加をニトロプルシッドで直接的に再現した場合にもVIP受容体結合は抑制されたが、この場合は主として低親和性結合部位の抑制によるものであり、CCKによる制御機構の本態とは考えられなかった。

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