作者: Michael C. Braun , Rose Y. Reins , Tong-bin Li , Travis J. Hollmann , Ranjan Dutta
DOI: 10.4049/JIMMUNOL.173.6.4190
关键词: In situ hybridization 、 Western blot 、 Receptor 、 Complement system 、 Anaphylatoxin 、 C3a receptor 、 Biology 、 Kidney 、 Microarray analysis techniques 、 Molecular biology
摘要: Although complement activation and deposition have been associated with a variety of glomerulopathies, the pathogenic mechanisms by which directly mediates renal injury remain to be fully elucidated. Renal parenchymal tissues express limited repertoire receptors that bind activated proteins. We report expression receptor for C3 cleavage product C3a, member anaphylatoxin family. C3aR is highly expressed in normal human murine kidney, as demonstrated immunohistochemistry situ hybridization. Its distribution epithelial cells only, glomerular endothelial mesangial showed no evidence expression. The also primary proximal tubular vitro FACS, Western blot, RT-PCR. In functional terms its capacity 125I-labeled C3a generate inositol triphosphate. Finally, using microarray analysis, four novel genes were identified confirmed transcriptionally regulated cells. These studies define new pathway may modulate response immunologic injury.