Lods J S, Nolet B, Morisset J
Département de biologie, Faculté des sciences, Université de Sherbrooke, Québec, Canada.
Biochem Biophys Res Commun. 1995 Jan 26;206(3):870-7. doi: 10.1006/bbrc.1995.1124.
The effects of pancreatic acinar cell desensitization by carbamylcholine (Cch), caerulein (Cae) and the phorbol ester TPA on the production of inositol tris and tetrakisphosphates were studied. In control acini, Cch and Cae caused comparable increases in Ins (1,4,5) P3, Ins (1,3,4,5) P4 and Ins (1,3,4) P3 after 15 sec stimulation. Desensitization by Cch totally inhibited the subsequent production of all three inositol phosphates in response to Cch. Desensitization by Cae allowed a subsequent production of all three inositol phosphates in response to Cae, but with a significant reduction. Desensitization by TPA reduced the production of Ins (1,4,5) P3 in response to Cch and Cae and totally inhibited that of the two other inositides. These data point to phospholipase C as a prime target for the altered production of inositol phosphates.
研究了氨甲酰胆碱(Cch)、蛙皮素(Cae)和佛波酯TPA对胰腺腺泡细胞脱敏作用对肌醇三磷酸和四磷酸生成的影响。在对照腺泡中,刺激15秒后,Cch和Cae使肌醇-1,4,5-三磷酸(Ins (1,4,5) P3)、肌醇-1,3,4,5-四磷酸(Ins (1,3,4,5) P4)和肌醇-1,3,4-三磷酸(Ins (1,3,4) P3)产生类似程度的增加。Cch引起的脱敏作用完全抑制了随后对Cch刺激产生的所有三种肌醇磷酸的生成。Cae引起的脱敏作用使随后对Cae刺激产生的所有三种肌醇磷酸仍能生成,但显著减少。TPA引起的脱敏作用降低了对Cch和Cae刺激产生的Ins (1,4,5) P3的生成,并完全抑制了另外两种肌醇磷脂的生成。这些数据表明磷脂酶C是肌醇磷酸生成改变的主要靶点。