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Studies On The Function Of Endothelial Cell And Its Regulation By Catechins

Posted on:2005-02-23Degree:DoctorType:Dissertation
Country:ChinaCandidate:A M PangFull Text:PDF
GTID:1104360155967867Subject:Internal medicine hematology
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Vascular endothelial cells, characteristic of monolayer, between the circulating blood and surrounding vascular tissue, commit the pivotal role in the diverse pathologies such as thrombosis and hemostasis, inflammation and immunization, angiogenesis, radiation damage and atherosclerosis. The investigation of endothelial cells' function has been furthered due to the advance of several new technologies such as electron microscope, cell culture and molecular biology. Here, we intend to unravel the phenomenon of the alteration of endothelial cells' function in systemic autoimmunity disease and how epigallocatechin gallate(EGCG), the main componect of Catechins, regulates the function of vascular endothelial growth factor( VEGF).I The alteration of endothelial cells' function in the pathology of systemic autoimmune disease1 The role of anti-endothelial cell antibodies in the pathology of autoimmune diseaseEndothelial cells(ECs ) share manifold physiological functions and can express various allogeneic antigens such as ABO blood type antigens, human leukocyte antigens and endothelial-specific antigens as the antigen presenting cells. The phenotype's alteration of the endothelial-specific antigens, located on the surface of EC, can stimulate the production of anti-endothelial cell antibodies(AECA), which lurks in the process of antoimmune diseases associated with vasculitis, such as systemic lupus erythematosus(SLE), rheumatoid arthritis(RA) and polymyositis(PM).Thrombocytopenia is a common clinical symptom, which is classified as the immune thrombocytopenia and non-immune thrombocytopenia according to its relevancy to immune system. Immune thrombocytopenia occurs not only in the hematological diseases(e.g. idiopathic thrombocytopenic purpura ,ITP) but also in various autoimmune diseases, which are implicated in the impairments of the multi-organ functions , such as SLE, RA and et al. Some patients with SLE or RAwere misdiagnosed as ITP at the initial stage clinically. Here, we intend to fathom the role of AECA in the pathology of ITP.We established the cell-ELISA to detect the serum level of AECA with the human umbilical cord vein endothelial cell (HUVEC) as the antigen. 70 patients with ITP, 45 patients with SLE, 33 patients with RA and 32 patients with aplastic anemia(AA) and 50 healthy individuals as the normal controls were recruited in our study, and the results were evaluated comprehensively with the clinical data. The patients with ITP, SLE, and RA had significantly higher AECA[(0.553 ±0.209), (0.820 ± 0.1540, (0.814 ± 0.234)) than normal controls[(0.404 ± 0.128)](P<0.01)while no significant difference existed between the patients with AA[(0.412 ±0.042)] and normal controls(P>0.05),the AECA in the patients with SLE and RA is significantly higher than that of ITP(P<0.01). The positive rate of AECA in patients with SLE and RA [84.44%(38/45), 81.82%(27/33)]is significantly higher than that of ITP[22.57%(16/70)](P<0.01). The platelet count in the patients with AECA(+)ITP [(18.94 ± 8.43) X 109 /L] is significantly lower than that of AECA(-)ITP[(44.93 ± 17.04) X109 /L](P0.05). The expression of platelet membrane glycoprotein P-selectin is also inhibited significantly by EGCG.Regarding to the above results, it is demonstrated that EGCG can suppress the proliferation of malignant cells by inhibiting the autocrine of VEGF, and can inhibit the paracrine of VEGF by restraining the expression of endothelial cell integrin P 3 induced by TGF- P 1. Simultaneously, EGCG can hinder the platelet to release VEGF by suppressing the activation of platelet. Taking one with another, EGCG can perpetrate the inhibitory role in the angiogenesis in different ways.
Keywords/Search Tags:anti-endothelial cell antibodies, anti-integrin αvβ3 antibodies, autoimmune thrombocytopenia, P-selectin, MACE, Systemic Sclerosis, Behcet's disease, epigallocatechin gallate(EGCG), vascular endothelial growth factor(VEGF), integrin β3, plasma TXB2
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