The expression and significance of neuronal iconic proteins in podocytes.
Growing evidence suggests that there are many common cell biological features shared by neurons and podocytes; however, the mechanism of podocyte foot process formation remains unclear. Comparing the mechanisms of process formation between two cell types should provide useful guidance from the progress of neuron research. Studies have shown that some mature proteins of podocytes, such as podocin, nephrin, and synaptopodin, were also expressed in neurons. In this study, using cell biological experiments and immunohistochemical techniques, we showed that some neuronal iconic molecules, such as Neuron-specific enolase, nestin and Neuron-specific nuclear protein, were also expressed in podocytes. We further inhibited the expression of Neuron-specific enolase, nestin, synaptopodin and Ubiquitin carboxy terminal hydrolase-1 by Small interfering RNA in cultured mouse podocytes and observed the significant morphological changes in treated podocytes. When podocytes were treated with Adriamycin, the protein expression of Neuron-specific enolase, nestin, synaptopodin and Ubiquitin carboxy terminal hydrolase-1 decreased over time. Meanwhile, the morphological changes in the podocytes were consistent with results of the Small interfering RNA treatment of these proteins. The data demonstrated that neuronal iconic proteins play important roles in maintaining and regulating the formation and function of podocyte processes.
Department of Pathology, Key Laboratory of Molecular Medicine, Chinese Ministry of Education, Shanghai Medical College, School of Basic Medical Science, Fudan University, Shanghai, P.R. China.
Yu
Y
Sun
Department of Pathology, Weifang Medical University, Weifang, Shandong, P.R. China.
Hongxia
H
Zhang
Department of Pathology, Key Laboratory of Molecular Medicine, Chinese Ministry of Education, Shanghai Medical College, School of Basic Medical Science, Fudan University, Shanghai, P.R. China.
Ruimin
R
Hu
Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, P.R. China.
Jianyong
J
Sun
Department of Pathology, Key Laboratory of Molecular Medicine, Chinese Ministry of Education, Shanghai Medical College, School of Basic Medical Science, Fudan University, Shanghai, P.R. China.
Xing
X
Mao
Department of Pathology, Key Laboratory of Molecular Medicine, Chinese Ministry of Education, Shanghai Medical College, School of Basic Medical Science, Fudan University, Shanghai, P.R. China.
Zhonghua
Z
Zhao
Department of Pathology, Key Laboratory of Molecular Medicine, Chinese Ministry of Education, Shanghai Medical College, School of Basic Medical Science, Fudan University, Shanghai, P.R. China.
Qi
Q
Chen
Department of Pathology, Key Laboratory of Molecular Medicine, Chinese Ministry of Education, Shanghai Medical College, School of Basic Medical Science, Fudan University, Shanghai, P.R. China.
Zhigang
Z
Zhang
D000818:Animals; D001921:Brain / Q000378:metabolism; D002460:Cell Line; D002478:Cells, Cultured; D015870:Gene Expression; D006801:Humans; D007668:Kidney / Q000378:metabolism; D051379:Mice; D064231:Nestin / Q000032:analysis* / Q000235:genetics; D009474:Neurons / Q000378:metabolism*; D009687:Nuclear Proteins / Q000032:analysis* / Q000235:genetics; D010751:Phosphopyruvate Hydratase / Q000032:analysis* / Q000235:genetics; D050199:Podocytes / Q000166:cytology / Q000378:metabolism*; D034622:RNA Interference; D051381:Rats; D017207:Rats, Sprague-Dawley
D064231:Nestin; D009687:Nuclear Proteins; D010751:Phosphopyruvate Hydratase