Meissner N N, Koschel K
Institut für Virologie und Immunbiologie, Universität Würzburg, Germany.
J Virol. 1995 Aug;69(8):5191-4. doi: 10.1128/JVI.69.8.5191-5194.1995.
Persistent infections of C6 rat astrocytoma cells with measles (subacute sclerosing panencephalitis [SSPE]) virus (C6/SSPE cells) or canine distemper virus (C6/CDV cells) cause a loss of endothelin-1 (ET-1) binding to its specific receptors (ETRA type) and subsequent ET-1-induced Ca2+ signaling. It was the aim of this study to investigate the underlying mechanism of this phenomenon in more detail. By using an RNase protection assay, it was found that ETRA mRNA disappears, whereas other cellular mRNA species, e.g., beta-actin mRNA, were not influenced. The data show that the loss of the ET-1 signaling pathway in C6/SSPE and C6/CDV cells is due to a receptor downregulation at the transcriptional level.
用麻疹（亚急性硬化性全脑炎[SSPE]）病毒（C6/SSPE细胞）或犬瘟热病毒（C6/CDV细胞）持续感染C6大鼠星形细胞瘤细胞，会导致内皮素-1（ET-1）与其特异性受体（ETRA型）的结合丧失，以及随后ET-1诱导的Ca2+信号传导丧失。本研究的目的是更详细地研究这一现象的潜在机制。通过使用核糖核酸酶保护试验，发现ETRA mRNA消失，而其他细胞mRNA种类，如β-肌动蛋白mRNA，未受影响。数据表明，C6/SSPE和C6/CDV细胞中ET-1信号通路的丧失是由于转录水平上的受体下调。
