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研究生:王心慧
研究生(外文):AriunaaSampilvanjil
論文名稱:基質金屬蛋白酵素在血管窄化誘發腹主動脈瘤之角色
論文名稱(外文):The role of matrix metalloproteinases in coarctation-induced abdominal aortic aneurysm
指導教授:江美治江美治引用關係
指導教授(外文):Meei-Jyh Jiang
學位類別:碩士
校院名稱:國立成功大學
系所名稱:細胞生物及解剖學研究所
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:2012
畢業學年度:100
語文別:英文
論文頁數:92
外文關鍵詞:Matrix MetalloproteinasesAbdominal Aortic AneurysmTIMPs
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Abdominal aortic aneurysm (AAA) is a common dilating disorder of the aorta and a major cause of death upon rupture. The key processes leading to AAA formation includes degradation of extracellular matrix (ECM), inflammation and smooth muscle cell (SMC) death. Our laboratory developed a coarctation-induced AAA model in Taiwanese Lanyu mini pigs characterized by high induction rate and elastic fiber degradation. Coarctation was performed in the infrarenal abdominal aorta (AA) for 4 weeks (4w), 8 weeks (8w), or 12 weeks (12w). AAA was detected in the AA segment distal to the coarctation at 12w post-coarctation. This study examined the role of matrix metalloproteinase-2 (MMP-2) and MMP-9 in the coarctation-induced AAA. The expression and activity of MMP-2 and MMP-9 were examined in three AA segments, i.e. suprarenal AA, proximal AA and distal AA. Suprarenal AA is located proximal to the renal arteries and is less likely to be affected by coarctation. Proximal AA is located proximal to the coarctation, which has laminar flow but is exposed to lower shear stress after coarctation. Messenger RNA levels, protein expression and activity levels of MMP-2 and MMP-9 were detected at 4w, 8w, and 12w post-coarctation with reverse transcription-polymerase chain reaction (RT-PCR), immunoblotting, and gelatinase zymography, respectively. In the distal AA segment, MMP-2 and MMP-9 mRNA levels were higher at 8w post-coarctation. Protein expression and activity levels of MMP-9 were higher at 4w post-coarctation while those of MMP-2 didn’t vary. In the proximal AA segment, MMP-2 mRNA expression was up-regulated throughout the experimental period but no change in protein expression and activity was detected after coarctation. MMP-9 activity was markedly higher at 8w post-coarctation. In the suprarenal AA segment, no difference in MMP-2 mRNA, protein or activity levels was detected between experimental and sham control groups whereas MMP-9 expression and activity were barely detectable. Comparison among the three AA segments revealed that both MMP-9 protein expression and activity in the distal AA were higher at 4w post-coarctation. Because MMP activities in vivo are regulated by tissue inhibitors of MMPs (TIMPs), the activities of TIMPs were examined by reverse zymography. The activities of TIMP-1, -2, -3, and -4 in all three AA segments did not change compared with the sham control. Interestingly, the proximal AA segment showed higher TIMP activity compared with other AA segments. TIMPs inhibit MMPs by forming 1:1 enzyme-inhibitor complex. Therefore, we assessed MMP/TIMP ratios to determine effective activity levels of MMP-2 and -9. In the distal AA segment, MMP-2/TIMP-2 and MMP-9/TIMP-3/4 ratios were elevated at 4w post-coarctation compared with sham control. Furthermore, MMPs/TIMPs ratios in the distal AA segment were higher than those of the other AA segments. Interestingly, in sham group, the distal AA also exhibited higher MMP-2/TIMP-2 and MMP-2/TIMP-3/4 ratios compared with other two AA segments. Plasmin activity is essential for MMPs activation and plasmin activator uPA plays important role in AAA formation, thus, we examined mRNA expression of uPA and tPA. In the distal AA segment, uPA mRNA levels increased at 4w post-coarctation and were higher than those of other AA segments. In contrast, tPA mRNA expression did not differ among AA segments and treatment groups. These results suggest that MMP-2 and -9 in combinations with TIMPs play important roles in the coarctation-induced AAA formation.
ACKNOWLEDGEMENTS -I
ABSTRACT -II
TABLE OF CONTENTS -IV
LIST OF FIGURES-VII
CHAPTER ONE INTRODUCTION -1
1.1 Abdominal aortic aneurysm -1
1.2 Structural properties of the normal aorta and their role in AAA -2
1.3 Pathogenesis and risk factors of the AAA -4
1.4 Histopathologic features of the AAA -5
1.5 The role of extracellular matrix degradation in AAA -6
1.5.1 Matrix metalloproteinase-2: Structure, activation and regulation -7
1.5.2 Matrix metalloproteinase-9: Structure, activation and regulation -9
1.5.3 Tissue inhibitors of metalloproteinases (TIMPs)-11
1.6 Medial smooth muscle cell loss in AAA -12
1.7 Animal models in AAA -12
CHAPTER TWO RESEARCH OBJECTIVE -14
CHAPTER THREE MATERIALS AND METHODS -15
3.1 Materials: -15
3.1.1 Experimental animals -15
3.1.2 Chemicals -16
3.1.3 Solution preparation -20
3.2 Methods:-28
3.2.1 RNA extraction and reverse transcription polymerase chain reaction (RT-PCR)-28
3.2.2 Extraction of gelatinases from aortic tissue -32
3.2.3 Western blotting -32
3.2.4 Gelatin zymography -36
3.2.5 Casein zymography -38
3.2.6 Reverse zymography -39
3.2.7 TUNEL staining -41
3.2.8 Statistic analysis -42
CHAPTER FOUR RESULTS -43
4.1 Coarctation-induced AAA formation -43
4.2 Changes in elastic lamellae during AAA formation -43
4.3 MMP-2 and MMP-9 expression and activity in the suprarenal AA segment -44
4.4 MMP-2 and MMP-9 expression and activity in the proximal AA segment -44
4.5 MMP-2 and MMP-9 expression and activity in the distal AA segment -45
4.6 MMP-2 and MMP-9 expression and activity comparison among different AA segments -45
4.7 Coarctation didn't change TIMPs activity in AA segments -46
4.8 MMP/TIMP ratios are increased in the distal AA segment -46
4.9 Coarctation increased uPA mRNA expression in the distal AA segment -47
4.10 Plasma levels of MMP-2 and -9 gelatinase activity after coarctation -48
4.11 The effect of coarctation on cell apoptosis in AA segments -48
CHAPTER FIVE DISCUSSION -49
REFERENCES -55
FIGURES -70
APPENDICES -92
Appendix 1: -92
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