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The Expression and Significance of Metalloproteinase and Apoptosis in the Calcific Aortic Valve

Author: ZhaoJianFeng
Tutor: QiGuoQi
School: Hebei Medical University
Course: Surgery
Keywords: Aortic Calcify Matrix metalloproteinase Apoptosis Immunohistochemical staining Electron microscopy
CLC: R654.2
Type: Master's thesis
Year: 2008
Downloads: 48
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Abstract

Heart valve disease is a common disease of our country, the country's aging population gradually increased, with the average life expectancy of raising the level of our national life and health, clinical aortic valve calcification in the treatment of elderly patients need surgery increased significantly. Heart valve calcification is not only caused by valvular abnormalities, can lead to heart failure, infective endocarditis, conduction block, thromboembolism, and even sudden death. As early as in the early twentieth century the famous pathologist Monckeberg aortic calcification is a rheumatic fever or aging passive pathological process, through a large number of studies in the past few decades, the etiology of aortic valve calcification mechanism a significant change has occurred. There are studies that aortic valve calcification is an active process of chronic inflammatory reaction, Mechanism and pathogenesis of aortic valve calcification is unclear. In recent years, with apoptosis and matrix metalloproteinase depth, apoptosis and matrix metalloproteinase understanding of the role in bone development may play an important role in the formation of aortic valve calcification. Matrix metalloproteinase is a group of zinc-dependent endopeptidase secreted form of zymogens can degradation of extracellular matrix components, including fibrillar collagen, including all its own inhibitory factor to influence by the balancing effect of the activation and expression tissue remodeling. Apoptosis is a form of cell death, the morphological features of cell shrinkage, nuclear fragmentation and chromatin condensation, apoptosis is a need for many enzymes involved in energy process. The study confirmed the pathological process involved in many cardiovascular diseases, apoptosis and apoptosis may play an important role in tissue remodeling process. Purpose: The purpose of this experiment is to study the matrix metalloproteinase -2 (MMP-2) and tissue inhibitor of metalloproteinase (TIMP-2) and the role of apoptosis in degenerative aortic valve calcification pathological process, preliminary study of aortic valve calcification occurrence of pathological mechanisms, to provide a theoretical basis for future prevention and treatment of aortic valve calcification. Method: drawn through clinical surgery for 15 cases of degenerative calcified aortic valve and 10 cases of non-calcified aortic valve, is divided into the the calcified group and non-calcified group, two groups of valvular immunohistochemical staining, TUNEL detection, and application of light mirror electron microscopy of two sets of valve morphology was observed, the study of calcified valves and non-calcified aortic valve matrix metalloproteinase -2 (MMP-2) and its tissue inhibitor (TIMP-2) expression and apoptosis, and change in the light microscope electron microscope observation of two sets of valve ultrastructure. Results: 1 light microscope calcified valvular collagen fibers dense edge blur, disorganized visible myxoid degeneration, lipid aggregation, karyopyknosis reduce disintegration of elastic fibers, tiny calcium salts are deposited at the bottom of the valve base first, collagen fibers myxoid degeneration and lipid accumulation region, to reduce the endodermis uneven, the integrity of the damage, the number of endothelial cells. Noncalcified valvular collagen fibers arranged in neat, the number of endothelial cells within the cortex integrity. 2 Immunohistochemical results showed that calcification of the aortic extracellular matrix and cell density increased significantly within the subcortical seen a lot of brown particles, MMP-2, TIMP-2, the positive cells were significantly more severe coloration, elongated the shaped or stellate distribution in the extracellular matrix and within subcortical parts. The noncalcified the valvular only visible scattered brown particles dispersed in the extracellular matrix, MMP-2, TIMP-2 positive cells, the number of small and light color. Comparing two sets of expression of MMP-2, TIMP-2 expression in the case, P <0.01 difference was significant. TUNEL assay, aortic calcification than non-calcified valvular number of apoptotic cells increased significantly, the mean apoptotic index in 9.07 vs0.21 0.71 ± ± 6.83 (P <0.05), the difference was statistically significant. Electron microscopy calcified aortic tissue cellular components in the valve significantly reduce, the fiber cell shrinkage grow fusiform karyopyknosis cytoplasm visible degeneration of mitochondria and vacuoles residual extracellular matrix visible more matrix vesicles, interstitial calcification and aggregation. The endothelial injury fragmentation from the focal individual endothelial cells into whole endothelial extensive exfoliative varying degrees, especially in the face of valvular aortic Valvular endothelial cells calcification and fibroblast nuclei appeared apoptosis, apoptotic cells important nuclear chromatin and cytoplasmic concentration, calcium deposition was observed in the apoptosis of fibroblast cell debris. Degradation product and organelles involved in calcium the valvular tissue calcification matrix material. Conclusion: MMP-2, TIMP-2 in the abnormal expression of destruction of extracellular matrix synthesis and degradation balance, increased matrix degradation;, including MMP-2, TIMP-2 aggregation subcutaneous endothelial damage, it not only affects the matrix retire The change is also involved in matrix remodeling. 2 aortic valve apoptosis of fibroblasts and endothelial injury severity is closely related apoptosis undermines the integrity of the endothelial cells, so that the filtration of calcium increase and deposited onto the valve tissue deep. 3 apoptosis of fibroblast cells to produce the cell debris, the degradation product provides a basis material for the calcium-binding, and promote the progress of valvular calcification. 4 matrix metalloproteinase activation and regulation in the calcified valve mechanism is not clear, modern molecular We also need to further clarify the activation mechanism of apoptosis leads to calcification, these problems will be doing further research.

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