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A peptide fragment of beta cardiac myosin heavy chain (beta-CMHC) can provoke autoimmune myocarditis as well as the corresponding alpha cardiac myosin heavy chain (alpha-CMHC) fragment.

机译:β心脏肌球蛋白重链(β-CMHC)的肽片段以及相应的α心脏肌球蛋白重链(α-CMHC)片段均可引起自身免疫性心肌炎。

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摘要

The validity of the general belief that alpha cardiac myosin heavy chain (alpha-CMHC) is primarily responsible for causing experimental autoimmune myocarditis because of the more profound tolerance induction to beta-CMHC due to its expression during the embryonic stage has been examined. In order to completely avoid cross-contamination among components of the two myosin heavy chains, recombinant myosin fragments were synthesized in Escherichia coli using cDNA fragments of rat alpha- and beta-CMHC cloned by reverse transcription polymerase chain reaction (RT-PCR). Two fragments corresponding to amino acid residues 1107-1164 derived from alpha- and beta-heavy chains were equally capable of provoking severe myocarditis in Lewis rats when immunized in complete Freund's adjuvant. No significant differences in the severity, as judged from histological scoring, were observed between the diseases induced by the two different peptide fragments, indicating conclusively that beta-CMHC is as pathogenic as alpha-CMHC.
机译:人们已经检验了人们普遍认为α心脏肌球蛋白重链(α-CMHC)主要是引起实验性自身免疫性心肌炎的有效性,因为由于其在胚胎期的表达,它对β-CMHC的耐受性更强。为了完全避免两条肌球蛋白重链的组分之间的交叉污染,使用通过逆转录聚合酶链反应(RT-PCR)克隆的大鼠α-和β-CMHC的cDNA片段在大肠杆菌中合成了重组肌球蛋白片段。在完全弗氏佐剂中免疫后,相当于衍生自α和β重链的氨基酸残基1107-1164的两个片段同样能够引发Lewis大鼠严重的心肌炎。根据组织学评分判断,在两种不同的肽片段诱导的疾病之间没有观察到严重程度的显着差异,最终表明,β-CMHC与α-CMHC一样致病。

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