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研究生:王來
研究生(外文):Lai Wang
論文名稱:兔子抗心脂質抗體與腺二磷酸或膠原蛋白協合活化人類血小的機制
論文名稱(外文):The mechanism of synergistic activation of human platelets by
指導教授:王 成 德
指導教授(外文):Cheng-teh Wang
學位類別:博士
校院名稱:國立清華大學
系所名稱:生命科學系
學門:生命科學學門
學類:生物學類
論文種類:學術論文
論文出版年:2002
畢業學年度:90
語文別:中文
論文頁數:157
中文關鍵詞:血小板抗心脂質抗體腺二磷酸膠原蛋白
外文關鍵詞:plateletanticardiolipin antibodiesADPcollagen
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摘 要
抗磷脂質抗體包括狼瘡性抗凝體與抗心脂質抗體,二者均為抗磷脂質症候群在血清診斷上的指標。抗磷脂質症候群的出現會引發血栓、續發性流產及血小板減少等至少之一的病症。而其中的動脈血栓被認為與血小板的活化有關。因此本論文的研究目標乃在探討抗心脂質抗體 anticardiolipin antibodies (ACLA) 以及 ACLA 與生理刺激劑 ADP 和 collagen 共同活化血小板時生化訊息傳遞的路徑。
在 ACLA 活化血小板時訊息傳遞路徑的探討上,我們先比較抗磷脂質抗體 ACLA 與 antiphosphatidylserine antibody (APSA) 的性質。APSA 與 ACLA 在下列的比較上相似 : 1) 均可與 CL 和 PS 結合; 2) 不需要 2-GPI 幫助抗體與 PS 或 CL 的結合; 3)可以造成血小板凝集; 4) 活化血小板的生化反應; 5) 可以與細胞膜上分子量 67 kDa 的膜蛋白結合。因此 APSA 與 ACLA 在活化血小板的功能上相似。
在 ACLA 活化血小板時生化反應上, ACLA 可造成: 1) PA 形成; 2) 細胞內鈣離子的上昇; 3) myosine light chain 與 pleckstrin 的磷酸化; 4) serotonin 和 -thromboglobulin 的釋出。ACLA 不會造成 PLC2 的酪胺酸磷酸化 (tyrosine phosphorylation)。從免疫墨點法 (immunoblotting) 的分析, ACLA 會活化血小板的 tyrosine kinase,表現出與 thrombin 和 collagen 類似的時間波段性。PKC 抑制劑 Ro31-8220 及細胞內鈣離子箝合劑 BAPTA/AM 對 ACLA 活化血小板時 tyrosine kinase 表現的影響是完全抑制.。 然而, 卻只有部分抑制 collagen 對 tyrosine kinase的活化。ACLA 也會對 PGE1 所引發的 cAMP 上昇產生 30% 抑制。以上結果可推論 ACLA 活化血小板可能是經由兩種訊息傳遞路徑而活化血小板。 一是 ACLA 活化 Gi 而抑制 adenylyl cyclase; 另一是活化Gq —PLC。
低濃度的 ADP 和 ACLA 可以彼此加強對血小板的活化。外加 fibrinogen 對 ADP 和 ACLA 使血小板的凝聚是必須的。生化測量上myosine light chain 與 pleckstrin 的磷酸化有協同性的高度上昇; 而細胞內鈣離子的上昇與顆粒體釋出則是加成性的增加。另外,tyrosin kinase 的活性也增強,fibrinogen 受體 integrin IIb3 (GPIIb-IIIa) 也有協同的增強而被暴露。 ADP P2Y1 受體之拮抗劑 A2P5P, 會抑制 integrin IIb3 (GPIIb-IIIa) 的活化。 ADP 和 ACLA 也抑制 PGE1 對血小板所引發的 cAMP 上昇。 由上述的結果可推論: ACLA 和 ADP 共同活化血小板時可使得 PKC 和PTK 活性增強因而讓fibrinogen 受體 IIbIIIa 被活化而暴露,這可能是當ADP 與 ACLA 共同活化血小板的關鍵反應。
低濃度 collagen 與 ACLA 可對血小板產生加強性活化。先加入 ACLA 到GFP, 5分鐘後再加入 collagen (ACLA + Col) 會看到協同性增強的反應包括凝集鈣離子濃度上昇與血小板凝集; 然而,若先加入 collagen,間隔超過1 分鐘再加入ACLA (Col+ACLA),則在1) myosine light chain 與 pleckstrin 的磷酸化; 2) -與 dense顆粒體的分泌,兩種反應程度減弱 30%。 抑制劑indomethacin 會抑制 (ACLA+Col) 所引發的細胞內鈣離子濃度上昇, pleckstrin 的磷酸化與血小板凝集。 在 thromboxane B2 的測量上, (ACLA+Col) 與 單獨 collagen 刺激血小板,兩者產量相近。(ACLA+Col) 活化血小板時會使得 PA 增加, 而抑制劑 indomethacin 與 A2P5P 會抑制 PA 的生成。由以上的結果可知 ACLA 與來自collagen 的 TXA2 和釋出的 ADP 共同加強 phospholipase C 的活性,而導致血小板的凝集。
綜合上述結果所得到的結論如下: ACLA 活化血小板可能經由兩種訊息傳遞路徑而活化血小板。 一是ACLA 活化 Gi 而抑制 adenylyl cyclase; 另一是活化Gq —PLC。 ACLA 和 ADP 共同活化血小板時可使得 PKC 和PTK 活性增強而讓fibrinogen 受體 IIb3 被活化而暴露,這可能是ADP 與 ACLA 共同活化血小板的關鍵。在ACLA 與collagen 共同活化血小板的反應上,ACLA 與來自collagen 的 TXA2 和釋出的 ADP 共同加強 phospholipase C 的活性,而導致血小板的凝集。
Abstract
Antiphospholipid antibodies include lupus anticoagulants and anticardiolipin antibodies (ACLA) which are the serological markers for antiphospholipid syndromes (APS). Patients of APS have at least one of the clinical features of venous thrombosis, arterial thrombosis, recurrent pregnancy loss, and thrombocytopenia. Platelet activation may have a role in APS, particularly in arterial thrombosis. This study aims to elucidate the mechanism of human platelet activation by ACLA and the synergistic effect of ACLA on low concentrations of physiological agonists including ADP and collagen.
The function properties of anti-phosphatidylserine antibodies (APSA) and ACLA in the signaling pathways of platelet activation were investigated. APSA and ACLA showed the similar results to ACLA in several respects including: 1) the affinity to antigens CL and PS in ELISA test; 2) independent of 2GP1 for phospholipid binding in ELISA test. 3) activation of platelet aggregation; 4) biochemical events of platelet activation; 5) binding to a platelet membrane protein with an apparent molecular weight 67 kDa as revealed by Western blotting. Therefore, APSA and ACLA may have the similar functional capacity.
Biochemical events studies showed that platelets activation by ACLA in: 1) PA formatioin; 2) Ca2+-mobilization; 3) phosphorylations of myosin-light chain and pleckstrin; 4) secretion of serotonin, -thromboglobulin. Immunoprecipitation study showed that ACLA did not cause tyrosine phosphorylation of PLC2. ACLA induced protein-tyrosine phosphorylation of platelets in a time-dependent manner similar to those of activation by thrombin and collagen. Ro 31-8220, a inhibitor of protein kinase C and BAPTA/AM, a Ca2+-chelator, inhibited ACLA-induced protein-tyrosine phosphorylation in the fibrinogen-dependent and aggregation-dependent steps. However, these two agents did not abolish these two steps of protein-tyrosine phosphorylation in high concentration of collagen. ACLA also inhibited prostaglandin E1-induced cyclic AMP formation by 30%. These results suggested that ACLA-signaling might be mediated by two signaling pathways including the receptor-inhibitory guanidine triphosphatase (receptor-Gi) pathway and phospholipase C (PLC) pathway.
Low concentrations of ADP and ACLA cooperatively potentiated the activation of human gel-filtrated platelets (GFP). The addition of fibrinogen was required to cause synergistic aggregation induced by ADP and ACLA. Biochemical events studied showed that the synergism occurred in phosphorylation of both myosin light chain and pleckstin, whereas there was only additive increase in [Ca2+]i and granule secretions. were observed. Furthermore, tyrosine kinases activities and the exposure of fibrinogen receptors IIb3 were synergistically increased when platelet stimulated by ADP and ACLA. A2P5P, an antagonist of ADP P2Y1 receptor, attenuated the exposure of IIb3 induced by ADP and ACLA. The additive inhibition of prostaglandin E1-induced cyclic AMP formation by ACLA and ADP were also observed. These results suggested platelet activation by ACLA and ADP was mediated by elevation the activity of tyrosine kinase and protein kinase C, therefore exposing the fibrinogen receptor.
Low concentrations of collagen and ACLA also cooperatively potentiated human GFP. GFP were treated with ACLA for 5 min prior to exposure to collagen (ACLA + Col) exerting strong responses in cytosolic Ca2+-mobilization and cell aggregation; However, cells were treated with collagen for 1 min prior to ACLA (Col + ACLA) exhibiting responses to a lesser extent. The same pattern also occurred in biochemical events such as: 1) phosphorylation of pleckstrin and myosin light chain; and 2) secretion of - and dense granule. Indomethacin inhibited Ca2+-mobilization, pleckstrin phosphorylation and cell aggregation in platelet stimulated by (ACLA + Col). The thromboxane B2 level in platelets induced by (ACLA + Col) was similar to that stimulated by low concentration of collagen alone. (ACLA + Col) increased the activities of phospholipases C (PLC) as determined by formation of PA, whereas indomethacin and A2P5P, abrogated the PA formation. These results suggest that ACLA, thromboxane A2 derived from the collagen pathway and secreted ADP cooperatively augmented the PLC’s activities leading to platelet aggregation.
In conclusion, the receptor-inhibitory guanidine triphosphatase (receptor-Gi) pathway and the phospholipase C (PLC) pathway were complicated in the ACLA signaling increases in the activity of tyrosine kinases and protein kinase C triggered the exposure of fibrinogen receptor which may be the key points for platelet activation by ACLA and ADP. The studies of synergistic activation of ACLA and collagen also suggest ACLA, thromboxane A2 derived from the collagen pathway and secreted ADP cooperatively augment the PLC’s activities and lead to platelet aggregation.
目錄
頁數
中文摘要
英文摘要……………………………………………………… III
縮寫及中英文對照………………………………………………………………… VI
目錄……………………………………………………………… XI
圖目錄…………………………………………………………… XV
表目錄…………………………………………………………… XVII
第一章. 緒論………………………………………………………1
第一節. 一.抗磷脂質抗體症候群與抗磷脂質抗體…… …… 1
二.血液凝固系統………………………………………6
三.抗磷脂質抗體的抗原異質性與可能的致病機轉…10
第二節. 血小板的生理功能與內部構造………………………14
一.血小板的生理角色………………………………14
二血小板的內部構造…………………………………15
第三節. 血小板的活化反應與訊息傳遞系統…………………18
一.血小板的活化與凝集……………………………18
二.血小板的訊息傳遞系統…………………………19
甲.訊息傳遞過程…………………………19
乙.GTP-binding proteins 23
丙. PI-specific isozymes………………………… 24
丁.PLA2………………………………………………………………… 28
戊.PI-3-kinase…………………………………………… 29
己.酪胺酸磷酸化 (tyrosine phosphorylation) …32
第四節. 不同生理刺激劑活化血小板所牽涉到的訊息傳遞系統……35
一.TXA2……………………………………………………………………… 35
二.Collagen………………………………………………………………… 38
三.ADP……………………………………………………………………… 39
四.Thrombin………………………………………………………………… 40
第五節. 不同刺激劑協合活化血小板的介紹…………………42
第六節. 研究目的及方向……………………………………………………………… 43
第二章. 實驗方法與步驟……………………………………… 45
第一節. 實驗材料……………………………………………… 45
第二節. 實驗方法…………………………………………… 47
一. 血小板之製備……………………………… 47
二. 抗磷脂質抗體 (ACLA,APSA) 的製備及純化…48
甲. 抗磷脂質抗體 (ACLA,APSA)
的誘發抗原的製備及抗體的誘發… 48
乙 抗體 (ACLA, APSA) 的純化…………49
丙 酵素免疫分析法 (Enzyme inkedimmunoassay; ELISA) 測定磷脂質和 ACLA, APSA 抗體的鍵結活性……50
丁 血小板細胞膜的分離………………………51
三. 血小板之凝集研究……………………………………52
四. 細胞內自由鈣離子的測量……………………53
五. 測定 TXB2 與 cyclic AMP 含量……………54
六. 血小板顆粒體分泌之測定……………………55
七. 電泳平板膠片之製備…………………………56
八. 磷酸化之測定…………………………………57
甲.蛋白磷酸化測定…………………………57
乙. Phosphatidic acid 的分析……………58
九.免疫墨點法與免疫沉澱測定蛋白酪胺酸磷酸化………59
十.GP IIb-IIIa 活化分析………………………………62
十一.統計分析……………………………………………62
第三章 抗磷脂質抗體活化血小板訊號傳遞路徑之探討…………63
第一節. 緒言………………………………………………… 63
第二節. 實驗結果……………………………………………… 65
一.ACLA與 APSA 性質之比較………………………65
二.ACLA 活化血小板時生化反應的表現……………69
第三節. 討論…………………………………………………… 79
第四章.ACLA 和 ADP 共同活化人類血小板機制之探討………84
第一節. 緒言…………………………………………………… 84
一ADP活化血小板訊息傳遞路徑…………84
二Integrin IIb3 (GPIIb-IIIa)的活化…87
第二節. 實驗結果………………………………………… 88
一.ACLA和 ADP 活化血小板時凝集反應的表現…………88
二. ACLA和 ADP 刺激血小板時生化反應的變化…………88
     三. ACLA和 ADP 刺激血小板時蛋白質酪胺酸磷酸化的表現…93
     四.ACLA和 ADP 刺激血小板時對PGE1 誘發cAMP 生成的抑制 99
     五.血小板 fibrinogen 接受器 ( GPIIb/IIIa ) 的活化……99
第三節. 討論…………………………………………………… 103
第五章 低濃度 ACLA 與Collagen 共同活化血小板時訊息傳遞之探討 107
第一節. 緒言……………………………………………… 107
第二節. 實驗結果……………………………………………… 110
一. ACLA 與 collagen 作用在血小板的先後時間對
協同作用表現的影響………………………………110
二 比較ACLA+Col 及Col+ACLA 活化血小板時之生化
反應………………………………………………114
三 ACLA+Col 及Col+ACLA細胞內鈣離子濃度 [Ca2+]i
的變化情形……………………………………… 114
四Indomethacin 對ACLA+Col 及Col+ACLA 活化血
小板的影響… 118
五.低濃度collagen,ACLA 和ACLA + Col 分別活化
血小板時TXB2之定量…………………………… 118
六.低濃度ACLA 和collagen活化血小板時PLC 的活化120
七.A2P5P 對ACLA 和 Col 活化血小板的抑制……124
第三節. 討論…………………………………………………… 126
第六章. 結論…………………………………………………… 129
參考文獻………………………………………………………… 132
圖目錄
頁數
圖1-1A 血液凝固過程中階段式反應的流程圖………………………… 7
圖1-1B APLA 對血液凝固系統,血小板和內皮細胞的影響……………12
圖1-2 電子顯微鏡下血小板形態與構造圖…………………………… 16
圖1-3 血小板活化的程序………………………………………………19
圖1-4 血小板訊息傳遞路徑的示意圖…………………………………22
圖1-5 四種 phospholipase C isozyme 結構特徵示意圖……………25
圖1-6 哺乳動物 PI3ks 的分類及結構特徵示意圖……………………30
圖1-7 不同活化階段的血小板與細胞內蛋白酪胺酸磷酸化的對應比較34
圖1-8 TXA2 活化血小板之訊息傳遞路徑………………………………37
圖1-9 Thrombin 活化血小板的訊息傳遞路徑…………………………41
圖3-1 ACLA 與 APSA 對磷脂質CL, PS和PC結合能力之分析………66
圖3-2 比較 beta2GP1 對ACLA 與 APSA 與磷脂質 CL, PS
結合能力的影響………… 67
圖3-3 不同濃度的ACLA 活化膠濾型血小板時的凝集曲線圖……………………… 70
圖3-4 抑制劑 A2P5P與 Indomethacin 對 ACLA 活化血小板時
PA 形成之影響… 72
圖3-5 ACLA 活化血小板時蛋白酪胺酸磷酸化表現的時間效應…………74
圖3-6 比較抑制劑 Ro 31-8220 與 BAPTA/AM 對 ACLA,
collagen thrombin 活化血小板時蛋白酪胺酸磷酸化的表現…75
圖3-7 ACLA 對PGE1 引發血小板cAMP 合成之抑制……………………76
圖3-8 西方免疫墨點法測定ACLA對血小板膜蛋白的結合……………78
圖3-9 ACLA 活化血小板的訊息傳遞路徑………………………………83
圖4A ADP 活化血小板的訊息傳遞路徑………………………………86
圖4-1 低濃度的ACLA 與 ADP 活化膠濾型血小板的凝集曲線圖……89
圖4-2 低濃度的ACLA 與不同濃度ADP 活化膠濾型血小板的表現……91
圖4-3 低濃度的ACLA 與 ADP 活化膠濾型血小板的蛋白酪胺酸
磷酸化表現 ……………………………………………………94
圖4-4A 低濃度的ACLA 與 ADP 活化膠濾型血小板的蛋白酪胺
酸磷酸化表現的時間效應…………………………………………95
圖4-4B ADP 與ACLA 共同活化血小板引發特定蛋白酪胺酸磷酸化
在第三分鐘之增加倍率……………………………………………98
圖4-5 ACLA 與 ADP 對PGE1 引發血小板cAMP 合成之抑制……………100
圖4-6A 抑制劑 A2P5P與 Bis 1 對低濃度 ACLA 與 ADP 活
化血小板受體 (GPIIb/IIIa ) 之影響………………………… 101
圖4-6B 抑制劑 A2P5P與 Bis 1 對低濃度 ACLA 與 ADP
(GPIIb/IIIa ) 之影響………………………………… 102
圖4-7 ACLA 與 ADP 協合活化血小板的訊號傳遞路徑……………… 106
圖5A 血小板受collagen 刺激之訊息傳遞路徑…………………… 109
圖5-1A 不同濃度的ACLA 與 collagen (Col) 活化膠濾型
血小板時的凝集曲線圖 111
圖5-1B ACLA 與 collagen 加入血小板懸浮液之順序與
時間差 ( t) 對血小板凝集的影響 112
圖5-2 ACLA (7 g/ml) 與 collagen (2 g/ml)
加入膠濾型血小板之順序與時間差 ( t) 對血小板
最大凝集程度與凝集初速率的影響…………… 113
圖5-3A ACLA (7 g/ml) 與 collagen (2 g/ml)
加入膠濾型血小板之順序與時間差 ( t) 對血小板
之蛋白質磷酸化的影響……………………………… 115
圖5-3B ACLA (7 g/ml) 與 collagen (2 g/ml)
加入膠濾型血小板之順序與時間差 ( t) 對血小板
之顆粒體釋出的影響…………………………………… 116
圖5-4 ACLA 與 collagen 加入膠濾型血小板之順序
與時間差(t) 對 血小板之細胞內自由鈣離子
濃度 ([Ca2+]i)的影響………………………………… …… 117
圖5-5 ACLA 與 collagen 加入膠濾型血小板之順序與時間差
(t) 對血小板之 TXB2 合成的時間效應………………………121
圖5-6 Indomethacin 與A2P5P 對ACLA 與 collagen刺激
血小板時 PA 形成的抑制………………………………………………………………………… 122
圖5-7 ACLA 與 collagen 活化膠濾型血小板時 PLC gamma2
酪胺酸磷酸化的表現… 123
圖5-8 ACLA與collagen 協合活化血小板之訊息傳遞路徑…………… 128
表目錄
頁數
表1-1 抗磷脂症候群研究紀事………………………………………………3
表3-1 比較ACLA 與 APSA 活化血小板時生化反應之差異………………68
表3-2 不同濃度之 ACLA 活血小板時之凝集參數………………………71
表4-1 低濃度的ACLA 與 ADP 活化膠濾型血小板的凝集反應……………90
表4-2 低濃度的ACLA 與 ADP 活化膠濾型血小板之生化反應表現………91
表5-1 Indomethacin 對ACLA 與Col 共同活化血小板生化反應的影響119
表5-2 A2P5P對ACLA 與 Col 活化血小板時凝集和PA 生成的影響……125
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