作者: Q. Fan , Y. Xing , J. Ding , N. Guan , J. Zhang
关键词: Podocin 、 Immunology 、 Podocyte 、 Western blot 、 Biology 、 Renal glomerulus 、 RNA interference 、 Nephrin 、 Cell biology 、 Messenger RNA 、 Gene knockdown
摘要: The abnormality of a single podocyte molecule, caused by gene mutation, such as NPHS1 , NPHS2 CD2AP and ACTN4 can lead to the hereditary/congenital nephrotic syndromes (NS). Further studies suggested that more than one molecule were together involved in acquired or experimental NS. However, we do not know much on relationship among these molecules, molecular response induced change each protein remaining ones. We respectively knockdown nephrin, podocin, CD2AP, α -actinin-4 mRNA using reconstructed RNA interference vector – psiRNA-hH1GFPzeo mouse clone. behavior was revealed quantitative expression both at levels with RT-PCR Western blot, distribution detected confocal microscopy. With nephrin knockdown, only increased, whereas podocin showed no change. Contrarily, decreased, while increased. Nephrin, did -actinin-4, begetted reduction increment CD2AP. redistributions around predominant nuclear staining compared membrane surface control podocytes. Our data imply between four molecules is very complicated evidently different. There always an interaction molecules. normal localization would depend their quantity reactions them.