Open Access

WWC1 promotes podocyte survival via stabilizing slit diaphragm protein dendrin

  • Authors:
    • Ting Lin
    • Li Zhang
    • Shuangxin Liu
    • Yuanhan Chen
    • Hong Zhang
    • Xingchen Zhao
    • Ruizhao Li
    • Qianmei Zhang
    • Ruyi Liao
    • Zongshun Huang
    • Bin Zhang
    • Wenjian Wang
    • Xinling Liang
    • Wei Shi
  • View Affiliations

  • Published online on: October 4, 2017     https://doi.org/10.3892/mmr.2017.7708
  • Pages:8685-8690
  • Copyright: © Lin et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Previous studies have indicated that glomerular podocyte injury serves a crucial role in proteinuria during the process of chronic kidney disease. The slit diaphragm of podocytes forms the final barrier to proteinuria. Dendrin, a constituent of the slit diaphragm protein complex, has been observed to relocate from the slit diaphragm to the nuclei in injured podocytes and promote podocyte apoptosis. However, the exact mechanism for nuclear relocation of dendrin remains unclear. The expression of WWC1 in podocyte injury induced by lipopolysaccharides (LPS) or adriamycin (ADR) was detected by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR), western blotting and the immunofluorescence assay. The role of WWC1 in podocyte apoptosis was detected by knockdown of WWC1 and flow cytometry. The mRNA and protein expression levels of apoptosis‑associated genes Bcl‑2‑associated X (Bax) and Bcl‑2 were measured by RT‑qPCR and western blotting. The impact of WWC1 on dendrin nucleus relocation in vitro in podocytes was further evaluated by knockdown of WWC1. Expression of WWC1 significantly decreased in injured podocytes in vitro. The loss‑of‑function assay indicated that knockdown of WWC1 gene in vitro promoted podocyte apoptosis, accompanied with increased levels of the pro‑apoptotic protein Bax and decreased levels of the anti‑apoptotic protein Bcl‑2. Furthermore, the relocation of dendrin protein was significantly promoted by knockdown of the WWC1 gene. In conclusion, the study indicated that loss of WWC1 may contribute to podocyte apoptosis by inducing nuclear relocation of dendrin protein, which provided novel insight into the molecular events in podocyte apoptosis.

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December 2017
Volume 16 Issue 6

Print ISSN: 1791-2997
Online ISSN:1791-3004

2016 Impact Factor: 1.692
Ranked #19/128 Medicine Research and Experimental
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APA
Lin, T., Zhang, L., Liu, S., Chen, Y., Zhang, H., Zhao, X. ... Shi, W. (2017). WWC1 promotes podocyte survival via stabilizing slit diaphragm protein dendrin. Molecular Medicine Reports, 16, 8685-8690. https://doi.org/10.3892/mmr.2017.7708
MLA
Lin, T., Zhang, L., Liu, S., Chen, Y., Zhang, H., Zhao, X., Li, R., Zhang, Q., Liao, R., Huang, Z., Zhang, B., Wang, W., Liang, X., Shi, W."WWC1 promotes podocyte survival via stabilizing slit diaphragm protein dendrin". Molecular Medicine Reports 16.6 (2017): 8685-8690.
Chicago
Lin, T., Zhang, L., Liu, S., Chen, Y., Zhang, H., Zhao, X., Li, R., Zhang, Q., Liao, R., Huang, Z., Zhang, B., Wang, W., Liang, X., Shi, W."WWC1 promotes podocyte survival via stabilizing slit diaphragm protein dendrin". Molecular Medicine Reports 16, no. 6 (2017): 8685-8690. https://doi.org/10.3892/mmr.2017.7708