Effects Of CVB3 Encoding Protein On Expression Of H9C2 Inflammatory Related Factors In Rat Cardiomyocytes

Myocarditis is a cardiac disease associated with inflammation andinjury of the myocardium. Several viruses have been associated with myocarditis in humans. However, coxsackievirus B3is still considered the dominant etiological agent. The observed pathology in viral myocarditis is a result of cooperation or teamwork between viral processes and host immune responses at various stages of disease. Both innate and adaptive immune responses are crucial determinants of the severity of myocardial damage, and contribute to the development of chronic myocarditis and dilated cardiomyopathy following acute viral myocarditis.Decisive factors in CVB3that result in myocarditis as well as their cell biological and immunological pathogenesis remain unclear.During the process of our research, to begin with, a series of primers are designed according to certain relative conservative sequences of CVB3. Secondly, functional regions of CVB3genome, which contain potential pathologic sites concerning myocarditisare obtained by PCR. These regions are integrated into a whole sequence which is6555-nt in length coding2185amino acids. Compared with known sequences of CVB3, homologous data of both nucleotide and amino acid sequences cover more than99percent.Furthermore, by a method of gene cloning technology, the above gene regions that can interpret5mature proteins in virus are linked into pcDNA3.1(+), constructing a host of novel expression plasmids. After that, such plasmids is utilized to transfect myocardial cells(H9C2) so that a further analysis can be observed and investigated about the expression situation of intracellular cytokines. It is indicated that most inflammatory factors in cells remain stable but TGF-p" goes up in the cells treated with CVB3and constructive plasmids embodying VP4,2B,3C proteins.To sum up, our research discovers that certain viral mature proteins in CVB3is able to induce the expression of TGF-p". Recent researches depict that TGF-β is likely to play a key role in myocardial fibrosis. The target of our research is to obtain a further illustration concerning mechanisms and pathogenesis of CVB3-caused viral myocarditis in hopes of setting up a firm experimental foundation for VM therapy as well as innovative medicines’ research anddevelopment.