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研究生:張志宗
研究生(外文):Chiz-Tzung Chang
論文名稱:蛋白質糖化終產物對於腎皮質集尿小管細胞之鈉離子運輸及細胞體積的調節
論文名稱(外文):The regulation of sodium transport and cell volume control by advanced glycation end products in renal cortical collecting duct cells
指導教授:吳麥斯吳麥斯引用關係楊智偉楊智偉引用關係
指導教授(外文):Mai-Szu WuChih-Wei Yang
學位類別:博士
校院名稱:長庚大學
系所名稱:臨床醫學研究所
學門:醫藥衛生學門
學類:醫學學類
論文種類:學術論文
論文出版年:2007
畢業學年度:95
語文別:英文
論文頁數:114
中文關鍵詞:蛋白質糖化終產物腎皮質集尿小管細胞鈉離子運輸血清糖固醇反應性腎皮質集尿鈉離子糖尿病細胞株
外文關鍵詞:Advanced glycation end productsrenal cortical collecting duct cellsodium transportsystemtaiwansystemtaiwan
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糖尿病腎病變在台灣是造成尿毒症最常見的原因.因為鈉離造成及高血壓是常見的症狀.腎臟於糖尿病腎病變的病理變化為細胞的肥大,而病理機轉為許多訊息傳導路徑的失調.
腎素,血管升壓激素,醛固酮系統之活化,細胞激素及生長因子的合成 糖的堆積蛋白質糖化終產物糖化及氧化壓力都是造成糖尿病腎變的可能路徑 所有的病理基轉都直接或間接與長期的高血糖有關.蛋白質糖化終產物是糖類和生肽非酵素反應的糖化作用而形成,蛋白質糖化終極產物隨著年齡老化而增加.於糖尿病患者則是隨著時間及血糖而改變.愈來愈多證據顯示蛋白質糖化終極產物與糖尿病腎病變的形成有關.
腎皮質集尿管細胞是腎臟最終調節鈉離子平衡之所在.鈉離子經由極端的上皮細胞鈉離子通道進入細胞而由基底端之鈉,鉀幫浦出細胞. 醛固酮是腎皮質集尿管細胞鈉離子運輸最重要的調節因子,醛固酮會誘發許多可以調控鈉離子通道活性的蛋白質.其中最重要的是血清糖固醇反應性活化酶是一種色胺酸/絲胺酸活化酶,原先由大鼠之乳房腫瘤細胞所繁殖出來,後來被發現也可能許多其他細胞中所表現 在腎臟的表現主要是在遠端腎小管 而糖尿病老鼠血清糖固醇反應性活化酶的表現是上升的,許多活體內及活體外的研究已經顯示血清糖固醇反應性活化酶可以調節許多離子通道的功能.例如上皮鈉離子通道及腎外髓質鉀通道.藉著調節這些通道的功能,血清糖固醇反應性活化酶可以來調控鈉滯留及細胞體積.
我們研究了蛋白質糖化終產物對於糖尿病腎病變之鈉離子滯留及細胞體積的調節.利用老鼠腎皮質集尿管細胞的細胞株來當實驗模型, 這個細胞有高電阻緊密上皮細胞的特性,且會表現上皮鈉離子通道 及血清糖固醇反應性活化酶.我們利用人工合成的蛋白質糖化終產物來刺激老鼠腎皮質集尿管細胞,上皮鈉離子通道及血清糖固醇反應性活化酶之表現及活性都被激發.經由蛋白質糖化終產物刺激的細胞會有肥大的現象.
Diabetic nephropathy is the most prevalent cause of renal failure in Taiwan. Edema and hypertension as a result of sodium retention is the common manifestation. Pathologically kidney in diabetic nephropathy is characterized by cellular hypertrophy. The pathophysiological mechanisms of diabetic nephropathy result from multiple dysregulated pathways. Activation of renin angiotensin aldosterone system, stimulated production of cytokines and growth factors, accumulation of sorbitol, enhanced production of advanced glycation end product (AGE) and induction of carbonyl or oxidative stress are all possible pathways of diabetic nephropathy. All these mechanisms are directly or indirectly generated by high serum glucose levels. Advanced glycation end products are formed by non-enzymatic glycation reactions between sugars and polypeptides following long-term incubation. Advanced glycation occurs during normal aging and is enhanced in diabetes as a function of time and sugar concentration. Increasing evidence demonstrates that AGE is an important factor involved in the development of diabetic nephropathy.
Renal cortical collecting duct (CCD) is the main renal tubular segment responsible for final regulation of sodium homeostasis. Sodium enters CCD cells via apical ENaC and exits via basal Na,K-ATPase. Aldosterone in the main regulator of sodium transport in CCD. Aldosterone induces the expression several proteins which can affect the expression and function of sodium pump. Among the regulatory proteins, Serum and Glucocorticoid-Responsive Kinase 1 is by far the most important one.
Sgk1 is a serine/ theorine kinase originally cloned as an immediate gene regulated by serum and glucorticoid in rat mammary tumor cells and later found to be present in many cell types. In kidney, Sgk1 is mainly distributed in distal renal tubule cells and its expression is enhanced in diabetic mouse. In vivo and in vitro studies have shown that SGK1 can regulate the function of many ion channels such as the epithelial sodium channel ENaC or the renal outer medullary potassium channel (ROMK). By regulating the activation of these channels SGK1 may lead to sodium retention and affect cell volume regulation.
We investigated the role of AGE in the sodium retention and cell volume control in diabetic nephropathy. Immortalized mouse CCD cell line mkpCCDcl4 were used as experimental model. CCD cells were stimulated with in vitro synthesized AGE. There were up-regulation of ENaC and Sgk expression and activity. Cell volume also increased in cells cultured with AGE as compared with control cells. The underlining mechanisms were also explored.
Chapter I: General Introduction………………………………………..1
1.1 Diabetic mellitus and diabetic nephropathy…………………….1
1.2 Renal sodium transport………………………………………….7
1.3 Diabetic nephropathy and ENaC……………………………… 9
1.4 Cell volume control…………………………………………….10
1.5 Cell volume and diabetic nephropathy…………………………11
Chapter II: Rationale and objective……………………………………14
2.1 Rationale………………………………………………………...14
2.2 Objective………………………………………………………...15
Chapter III: Experiment I Establishment of experimental model and characterization of cell line used……………………………………….16
3.1 Introduction……………………………………………………...16
3.2 Material and methods……………………………………………16
3.3 Results of experiment I…………………………………………..21
3.4 Discussion………………………………………………………..27
Chapter IV: Experiment II The regulation of epithelial sodium transport by advanced glycation end products in mouse cortical collecting duct cells……………………………………………………………………..28
4.1 Introduction………………………………………………………28
4.2 Material and methods…………………………………………….28
4.3 Results of experiment II………………………………………….37
4.4 Discussion………………………………………………………..49
Chapter V: Experiment III The regulation of sodium transport of cortical collecting duct cells by transformation growth factor-………………..52
5.1 Introduction………………………………………………………52
5.2 Material and methods…………………………………………….54
5.3 Results of experiment III…………………………………………60
5.4 Discussion………………………………………………………...72
Chapter VI: Experiment IV Advanced glycation end products induced cortical collecting duct cells hypertrophy………………………………77
6.1 Introduction………………………………………………………77
6.2 Material and methods…………………………………………….79
6.3 Results……………………………………………………………83
6.4 Discussion………………………………………………………..95
Chapter VII: Conclusion in Chinese and English………………………97
結論……………………………………………………………………..97
Conclusion………………………………………………………………99
Future Direction………………………………………………………..101
Reference………………………………………………………………102
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