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P38MAPK Regulates The Changes Of Cardiac Microvascular Endothelial Cells Actin Cytoskeleton, Tight Junction And Permeability Caused By Coxsackievirus B3

Posted on:2007-07-03Degree:MasterType:Thesis
Country:ChinaCandidate:D F ShaoFull Text:PDF
GTID:2144360185482849Subject:Pathology and pathophysiology
Abstract/Summary:PDF Full Text Request
Objectives:The group B of Coxsackieviruses ( CVB) belongs to enterovirus of family picornavirus. There are six serotypes in CVB, which are CVB1 to 6 particularly CVB3 are considered to be the most frequent cause of human viral heart disease. It is estimated more than 20% of cases of viral myocarditis are caused by CVB3, and viral myocarditis can induce severe arrhythmia and sudden cardiac death and lead to the development of a chronic form of myocarditis, dilated cardiomyopathy, which is the second leading etiological cause of heart transplantation. CVB3 infections are characterized by primary viral replication at the portal of entry, such as the nasopharynx and intestine, and then viruses into the bloodstream which is called viremia, via the blood during viremia, CVB3 can invade several different organs which distant from the gut, such as heart, pancreatic islet and central nervous system and so on, causing myocarditis, pancretitis or viral meningitis.Viruses must either pass through the vascular endothelium by transcytosis or infection or be carried past the endothelial barrier by infected circulating cells, which can migrate into the target tissues, In fact, two such events must occur, since the virus must enter into the circulation first and then leave the circulation to gain access to the secondary sites of infection. Therefore, CVB3 must induce endothelial barrier dysfunction during the process to get through the endothelial cells. Cardiac...
Keywords/Search Tags:Coxsackievirus, Cardiac microvascular endothelial cells, cytoskeleton, tight junction, F-actin, ZO-1, permeability, p38 MAPK
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