Rubio Nazario, Sanz-Rodriguez Francisco
Instituto Cajal. C.S.I.C, Dr. Arce Avenue 37, 28002, Madrid, Spain.
Department of Biology, Universidad Autonoma de Madrid, Madrid, Spain.
J Neurovirol. 2016 Jun;22(3):316-26. doi: 10.1007/s13365-015-0400-9. Epub 2015 Nov 13.
In this study, we demonstrate the upregulation in the expression of caspases 1 and 11 by SJL/J mouse brain astrocytes infected with the BeAn strain of Theiler's murine encephalomyelitis virus (TMEV). The upregulation of both proteases hints at protection of astrocytic cells from apoptotic death. We therefore looked for the reason of the demonstrated absence of programmed cell death in BeAn-infected SJL/J astrocytes. Complementary RNA (cRNA) from mock- and TMEV-infected cells was hybridized to the whole murine genome U74v2 DNA microarray from Affymetrix. Those experiments demonstrated the upregulation of gene expression for caspases 1 and 11 in infected cells. We further confirmed and validated their messenger RNA (mRNA) increase by reverse transcriptase quantitative real-time PCR (qPCR). The presence of both enzymatically active caspases 1 and 11 was demonstrated in cell lysates using a colorimetric and fluorymetric assay, respectively. We also show that overexpressed caspase 11 activated caspase 1 after preincubation of cytosol in vitro following a time-dependent process. This induction was neutralized by an anti-caspase 11 polyclonal antibody. These results demonstrate the activation of the caspase 1 precursor by caspase 11 and suggest a new mechanism of protection of BeAn-infected astrocytes from apoptosis. The direct experimental evidence that the protection effect demonstrated in this article was mediated by caspase 1, is provided by the fact that its specific inhibitor Z-WEHD-FMK induced de novo apoptotic death.
在本研究中,我们证明了感染泰勒氏鼠脑脊髓炎病毒(TMEV)BeAn株的SJL/J小鼠脑星形胶质细胞中,半胱天冬酶1和11的表达上调。这两种蛋白酶的上调表明星形胶质细胞受到保护,免于凋亡死亡。因此,我们探究了在感染BeAn的SJL/J星形胶质细胞中程序性细胞死亡缺失的原因。将来自未感染和TMEV感染细胞的互补RNA(cRNA)与Affymetrix公司的全小鼠基因组U74v2 DNA微阵列杂交。这些实验证明了感染细胞中半胱天冬酶1和11的基因表达上调。我们通过逆转录定量实时PCR(qPCR)进一步证实并验证了它们信使RNA(mRNA)的增加。分别使用比色法和荧光法在细胞裂解物中证实了具有酶活性的半胱天冬酶1和11的存在。我们还表明,在体外将细胞溶质预孵育后,过表达的半胱天冬酶11会在一个时间依赖性过程后激活半胱天冬酶1。这种诱导作用被抗半胱天冬酶11多克隆抗体中和。这些结果证明了半胱天冬酶11对半胱天冬酶1前体的激活,并提示了一种保护感染BeAn的星形胶质细胞免于凋亡的新机制。本文所证明的保护作用是由半胱天冬酶1介导的直接实验证据是,其特异性抑制剂Z-WEHD-FMK诱导了新的凋亡死亡。