小鼠胰腺腺泡细胞系MPC-83中功能性G蛋白偶联受体的缺失  

Complete loss of functional G protein-coupled receptors in mouse pancreatic acinar cell MPC-83

作　　者：程海立[1] 王琳[1] 崔宗杰[1] 

机构地区：[1]北京师范大学细胞生物学研究所,北京市100875

出　　处：《世界华人消化杂志》2008年第6期590-595,共6页World Chinese Journal of Digestology

基　　金：国家自然科学基金;No.30472048;No.3054042524;北京市自然科学基金;No.6062014~~

摘　　要：目的:研究小鼠胰腺肿瘤细胞系MPC-83细胞中功能性G蛋白偶联受体(G protein-coupled receptor,GPCR).方法:培养小鼠胰腺肿瘤细胞系MPC-83细胞,检测其刺激前后胞质游离钙离子浓度的变化.结果:ACh 25 nmol/L刺激新鲜分离的正常小鼠胰腺腺泡细胞,胞质钙离子浓度发生规则、振荡样升高:CCK 5 pmol/L具有类似作用.GPCR激动剂CCK 1μmol/L、VP 1μmol/L、P物质5μmol/L、组织氨10μmol/L、PE 10μmol/L和ACh 100μmol/L分别刺激MPC-83细胞,胞质钙离子没有发生任何增加.地塞米松100 nmol/L与MPC-83细胞共孵育72h,MPC-83细胞增殖速度明显降低,但GPCR配体CCK、VP、P物质仍然不引起胞质钙离子浓度的增加.结论:从昆明小鼠胰腺外分泌部肿瘤分离出来的胰腺腺泡细胞系MPC-83,正常的G蛋白偶联受体完全缺失,处于极度去分化状态.AIM：To study G-protein-coupled receptor （GPCR）in mouse exocrine pancreatic acinar cell line MPC-83. METHODS：Cytoplasmic calcium concentration in mouse exocrine pancreatic acinar cell line MPC-83 was measured both before and after stimulation with GPCR agonists. RESULTS：Acetylcholine（ACh,25 nmol/L）and cholecystokinin（CCK,5 μmol/L）induced regular calcium oscillations in freshly isolated normal mouse pancreatic acinar cells.When GPCR agonists CCK（1μmol/L）,vasopressin（VP,1μmol/L）,substance P（5μnol/L）,histamine（10μmol/L）,phenylephrine（PE,10μmol/L）and ACh 100μmol/L were added to MPC-83 cells, no change of intracellular calcium concentration was detected.After 100 nmol/L dexamethasone pre-treatment of MPC-83 cells for 72h,MPC-83 cell proliferation was reduced,but still no calcium increases were detected after stimulation with GPCR agonists 1μmol/L CCK,1μmol/L VP and 5μmol/L substance P. CONCLUSION：The pancreatic acinar tumor cell line MPC-83 from Kunming mice have completely lost their functional GPCR which are normally present in pancreatic acinar cells,and these cells are in extreme de-differentiation state.

关 键 词：胰腺腺泡细胞 G蛋白偶联受体 胞质钙振荡 FURA-2 去分化 MPC-83细胞 

分 类 号：R576[医药卫生—消化系统]