[Analysis of heterogeneity in exon 4 of Coxsackievirus and Adenovirus receptor gene in dilated cardiomyopathy].
Shuo Zhang, Lei Teng, Haibo Jia, Lili Li, Xueqin Gao, Bo Yu
Abstract
Shuo Zhang, Lei Teng, Haibo Jia, Lili Li, Xueqin Gao, Bo Yu
Abstract
OBJECTIVE: To investigate the genetic pathogenesis of dilated cardiomyopathy (DCM) by examining the heterogeneity of Coxsackievirus binding domain (exon 4) of Adenovirus receptor (CAR) in DCM patients and healthy adults, and to detect possible mutation site in exon 4. METHODS: Using polymerase chain reaction (PCR), we amplified exon 4 of CAR DNA extracted from blood samples obtained from 50 DCM patients and 40 healthy adults. The PCR products were screened with single-strand conformation polymorphism (SSCP) and then sequenced alternatively based on the SSCP results. RESULTS: The segment of CAR exon 4 was successfully amplified and there was no single strand conformational disparity in all samples examined by SSCP. Sequence analysis demonstrated that all amplified sequences of CAR exon 4 from samples of the two groups were identical and there was no genetic heterogeneity of CAR exon 4 between the two groups. CONCLUSION: The genetic heterogeneity of CAR exon 4 might not be responsible for the pathogenesis of DCM.
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OBJECTIVE: To investigate the genetic pathogenesis of dilated cardiomyopathy (DCM) by examining the heterogeneity of Coxsackievirus binding domain (exon 4) of Adenovirus receptor (CAR) in DCM patients and healthy adults, and to detect possible mutation site in exon 4. METHODS: Using polymerase chain reaction (PCR), we amplified exon 4 of CAR DNA extracted from blood samples obtained from 50 DCM patients and 40 healthy adults. The PCR products were screened with single-strand conformation polymorphism (SSCP) and then sequenced alternatively based on the SSCP results. RESULTS: The segment of CAR exon 4 was successfully amplified and there was no single strand conformational disparity in all samples examined by SSCP. Sequence analysis demonstrated that all amplified sequences of CAR exon 4 from samples of the two groups were identical and there was no genetic heterogeneity of CAR exon 4 between the two groups. CONCLUSION: The genetic heterogeneity of CAR exon 4 might not be responsible for the pathogenesis of DCM.
Key concepts: Exon, Single-strand conformation polymorphism, Dilated cardiomyopathy, Pathogenesis, Coxsackievirus, Polymerase chain reaction, Molecular biology, Mutation