Barwick Shannon R, Siddiq Mevish S, Wang Jing, Xiao Haiyan, Marshall Brendan, Perry Elizabeth, Smith Sylvia B
Department of Cellular Biology and Anatomy, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA.
James and Jean Culver Vision Discovery Institute, Augusta University, Augusta, GA 30912, USA.
Antioxidants (Basel). 2021 Jun 19;10(6):981. doi: 10.3390/antiox10060981.
Sigma 1 receptor (Sig1R), a modulator of cell survival, has emerged as a novel target for retinal degenerative disease. Studies have shown that activation of Sig1R, using the high affinity ligand (+)-pentazocine ((+)-PTZ), improves cone function in a severe retinopathy model. The rescue is accompanied by normalization of levels of NRF2, a key transcription factor that regulates the antioxidant response. The interaction of Sig1R with a number of proteins has been investigated; whether it interacts with NRF2, however, is not known. We used co-immunoprecipitation (co-IP), proximity ligation assay (PLA), and electron microscopy (EM) immunodetection methods to investigate this question in the 661W cone photoreceptor cell line. For co-IP experiments, immune complexes were precipitated by protein A/G agarose beads and immunodetected using anti-NRF2 antibody. For PLA, cells were incubated with anti-Sig1R polyclonal and anti-NRF2 monoclonal antibodies, then subsequently with (-)-mouse and (+)-rabbit PLA probes. For EM analysis, immuno-EM gold labeling was performed using nanogold-enhanced labeling with anti-NRF2 and anti-Sig1R antibodies, and data were confirmed using colloidal gold labeling. The co-IP experiment suggested that NRF2 was bound in a complex with Sig1R. The PLA assays detected abundant orange fluorescence in cones, indicating that Sig1R and NRF2 were within 40 nm of each other. EM immunodetection confirmed co-localization of Sig1R with NRF2 in cells and in mouse retinal tissue. This study is the first to report co-localization of Sig1R-NRF2 and supports earlier studies implicating modulation of NRF2 as a mechanism by which Sig1R mediates retinal neuroprotection.
西格玛-1受体(Sig1R)是一种细胞存活调节剂,已成为视网膜退行性疾病的新靶点。研究表明,使用高亲和力配体(+)-喷他佐辛((+)-PTZ)激活Sig1R,可改善严重视网膜病变模型中的视锥细胞功能。这种挽救伴随着关键转录因子NRF2水平的正常化,NRF2可调节抗氧化反应。人们已经研究了Sig1R与多种蛋白质的相互作用;然而,它是否与NRF2相互作用尚不清楚。我们使用免疫共沉淀(co-IP)、邻近连接分析(PLA)和电子显微镜(EM)免疫检测方法,在661W视锥光感受器细胞系中研究了这个问题。对于co-IP实验,免疫复合物用蛋白A/G琼脂糖珠沉淀,并用抗NRF2抗体进行免疫检测。对于PLA,细胞先用抗Sig1R多克隆抗体和抗NRF2单克隆抗体孵育,然后用(-)-小鼠和(+)-兔PLA探针孵育。对于EM分析,使用抗NRF2和抗Sig1R抗体的纳米金增强标记进行免疫电镜金标记,并用胶体金标记确认数据。co-IP实验表明NRF2与Sig1R结合形成复合物。PLA分析在视锥细胞中检测到大量橙色荧光,表明Sig1R和NRF2彼此距离在40纳米以内。EM免疫检测证实了Sig1R与NRF2在细胞和小鼠视网膜组织中的共定位。本研究首次报道了Sig1R-NRF2的共定位,并支持了早期研究,即NRF2的调节是Sig1R介导视网膜神经保护的一种机制。