Rehn Torben, Lubiana Pedro, Nguyen Thi Huyen Trang, Pansegrau Eva, Schmitt Marius, Roth Lisa Katharina, Brehmer Jana, Roeder Thomas, Cadar Dániel, Metwally Nahla Galal, Bruchhaus Iris
Bernhard Nocht Institute for Tropical Medicine, 20359 Hamburg, Germany.
Molecular Physiology Department, Zoological Institute, Christian-Albrechts University Kiel, 24118 Kiel, Germany.
Microorganisms. 2022 Jun 9;10(6):1183. doi: 10.3390/microorganisms10061183.
-infected erythrocytes (IEs) adhere to endothelial cell receptors (ECRs) of blood vessels mainly via EMP1 proteins to escape elimination via the spleen. Evidence suggests that -infected reticulocytes (IRs) also bind to ECRs, presumably enabled by VIR proteins, as shown by inhibition experiments and studies with transgenic expressing genes. To test this hypothesis, our study investigated the involvement of VIR proteins in cytoadhesion using gene-expressing transfectants. Those VIR proteins with a putative transmembrane domain were present in Maurer's clefts, and some were also present in the erythrocyte membrane. The VIR protein without a transmembrane domain (PVX_050690) was not exported. Five of the transgenic cell lines, including the one expressing PVX_050690, showed binding to CD36. We observed highly increased expression of specific genes encoding EMP1s in all CD36-binding transfectants. These results suggest that ectopic expression regulates expression through a yet unknown mechanism. In conclusion, the observed cytoadhesion of expressing genes depended on EMP1s, making this experimental unsuitable for characterizing VIR proteins.
受感染的红细胞（IEs）主要通过EMP1蛋白与血管内皮细胞受体（ECRs）结合，以逃避脾脏的清除。有证据表明，受感染的网织红细胞（IRs）也与ECRs结合，推测是由VIR蛋白介导的，这在抑制实验和表达基因的转基因研究中得到了证实。为了验证这一假设，我们的研究使用表达基因的转染子研究了VIR蛋白在细胞黏附中的作用。那些具有推定跨膜结构域的VIR蛋白存在于毛氏小体中，有些也存在于红细胞膜中。没有跨膜结构域的VIR蛋白（PVX_050690）没有输出。包括表达PVX_050690的细胞系在内的五个转基因细胞系显示出与CD36的结合。我们观察到在所有与CD36结合的转染子中，编码EMP1s的特定基因的表达高度增加。这些结果表明，异位表达通过一种未知机制调节表达。总之，观察到的表达基因的细胞黏附依赖于EMP1s，这使得该实验不适合用于表征VIR蛋白。
