Scn3b在遗传性糖尿病长爪沙鼠多种组织中的表达情况
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摘要
目的比较正常血糖长爪沙鼠和自发遗传性糖尿病长爪沙鼠肝脏、肾脏、骨骼肌和脑组织中钠通道β亚基(sodium channel beta subunit 3 gene,Scn3b)的表达差异。方法选取正常血糖长爪沙鼠和自发遗传性糖尿病长爪沙鼠各6只,分别采集动物的肝脏、肾脏、骨骼肌和脑组织,利用Real-time PCR和Western blotting检测Scn3b在各组织中的mRNA和蛋白表达水平。结果与正常血糖动物相比,在糖尿病长爪沙鼠肝脏和脑组织中,Scn3b mRNA和蛋白水平表达均下降,其中在肝脏具显著性差异。结论 Scn3b在糖尿病长爪沙鼠肝脏和脑组织中表达减少,提示在肝脏和脑组织中Scn3b的异常表达可能参与长爪沙鼠糖尿病的发生。
Objective To investigate the mRNA and protein expression level of sodium channel beta subunit 3 gene(Scn3b) in 4 tissues of spontaneous hereditary diabetic and non-diabetic gerbils. Method We selected 6 diabetic and 6 non-diabetic control gerbils,and collected liver,kidney,skeletal muscle and brain from each animal,respectively. The mRNA and protein expression of Scn3 b was evaluated by Real-time PCR and Western blotting in diabetic and non-diabetic control groups. Result Compared with control group,mRNA and protein expression of Scn3b reduced in liver and brain from diabetic gerbils,and the difference in liver between the two groups was statistical significant. Conclusion Scn3b expression decreased in liver and brain in diabetic gerbils,suggesting that Scn3 b in liver and brain may be involved in development of gerbil diabetes.
Objective To investigate the mRNA and protein expression level of sodium channel beta subunit 3 gene(Scn3b) in 4 tissues of spontaneous hereditary diabetic and non-diabetic gerbils. Method We selected 6 diabetic and 6 non-diabetic control gerbils,and collected liver,kidney,skeletal muscle and brain from each animal,respectively. The mRNA and protein expression of Scn3 b was evaluated by Real-time PCR and Western blotting in diabetic and non-diabetic control groups. Result Compared with control group,mRNA and protein expression of Scn3b reduced in liver and brain from diabetic gerbils,and the difference in liver between the two groups was statistical significant. Conclusion Scn3b expression decreased in liver and brain in diabetic gerbils,suggesting that Scn3 b in liver and brain may be involved in development of gerbil diabetes.
引文
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[12]Rorsman P,Braun M.Regulation of insulin secretion in human pancreatic islets[J].Annu Rev Physiol,2013,75:155-179.
[2]American Diabetes Association.Diagnosis and classification of diabetes mellitus[J].Diabetes Care,2004,27(Suppl 1):S5-S10.
[3]Ashcroft F M,Rorsman P.Diabetes mellitus and theβcell:the last ten years[J].Cell,2012,148(6):1160-1171.
[4]李长龙,杜小燕,郭萌,等.长爪沙鼠模型群体的培育[J].实验动物科学,2016,33(3):52-55,60.
[5]Catterall W A,Goldin A L,Waxman S G.International Union of Pharmacology.XLVII.Nomenclature and structure-function relationships of voltage-gated sodium channels[J].Pharmacol,2006,57(4):397-409.
[6]Jin W,Patti M E.Genetic determinants and molecular pathways in the pathogenesis of Type 2 diabetes[J].Clin Sci(Lond),2009,116(2):99-111.
[7]赵永梅,李敬华,李贺.外源性胰岛素对2型糖尿病内皮功能影响的研究进展[J].现代中西医结合杂志,2016,25(4):448-450.
[8]Ernst S J,Aguilar-Bryan L,Noebels J L,et al.Sodium channel beta1 regulatory subunit deficiency reduces pancreatic islet glucose-stimulated insulin and glucagon secretion[J].Endocrinology,2009,150:1132-1139.
[9]Zhang Q,Chibalina M V,Bengtssn M,et al.Na+current properties in islet alpha-and beta-cells reflect cell-specific Scn3a and Scn9a expression[J].J Physiol,2014,592:4677-4696.
[10]Eliasson L,Abdulkader F,Braun M,et al.Novel aspects of the molecular mechanisms controlling insulin secretion[J].J Physiol,2008,586:3313-3324.
[11]Mac Donald P E.Signal integration at the level of ion channel and exocytotic function in pancreatic b-cells[J].Am J Physiol Endocrinol Metab,2011,301:E1065-E1069.
[12]Rorsman P,Braun M.Regulation of insulin secretion in human pancreatic islets[J].Annu Rev Physiol,2013,75:155-179.