H2O2 induces caveolin‑1 degradation and impaired mitochondrial function in E11 podocytes

  • Authors:
    • Ya‑Hui Chen
    • Wei‑Wen Lin
    • Chin‑San Liu
    • Shih‑Li Su
  • View Affiliations

  • Published online on: September 18, 2017     https://doi.org/10.3892/mmr.2017.7497
  • Pages: 7841-7847
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Increased intercellular reactive oxygen species (ROS) levels are the major cause of podocyte injury with proteinuria. Caveolin‑1 (CAV‑1) is an essential protein component of caveolae. CAV‑1 participates in signal transduction and endocytic trafficking. Recent research has indicated that CAV‑1 regulates oxidative stress‑induced pathways. The present study used hydrogen peroxide (H2O2) at nontoxic concentrations to elevate the level of ROS in E11 podocytes. Treatment with 500 and 1,000 µM H2O2 for 1 h significantly reduced CAV‑1 expression levels. Simultaneously, the treatment significantly reduced the expression of the antioxidant enzymes glutamine‑cysteine ligase catalytic subunit, superoxide dismutase 2 and catalase. To determine the role of CAV‑1 in mediating oxidative stress, E11 podocytes were administered antenapedia‑CAV‑1 (AP‑CAV‑1) peptide for 48 h. The AP‑CAV‑1 treatment enhanced CAV‑1 expression and inhibited cyclophilin A expression, thus reducing ROS‑induced inflammation. Moreover, CAV‑1 protected against H2O2‑induced oxidative stress responses by enhancing the expression of antioxidant enzymes. Furthermore, CAV‑1 attenuated H2O2‑induced changes oxidative phosphorylation, and the expression of optic atrophy 1 and translocase of the inner membrane 23, as well as preserving mitochondrial function. CAV‑1 treatment significantly suppressed apoptosis, as indicated by a higher B‑cell lymphoma 2/BCL2‑associated X protein ratio. Therefore, enhancing the expression of CAV‑1 may be an important therapeutic consideration in treating podocyte injury.
View Figures
View References

Related Articles

Journal Cover

November-2017
Volume 16 Issue 5

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

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Chen YH, Lin WW, Liu CS and Su SL: H2O2 induces caveolin‑1 degradation and impaired mitochondrial function in E11 podocytes. Mol Med Rep 16: 7841-7847, 2017
APA
Chen, Y., Lin, W., Liu, C., & Su, S. (2017). H2O2 induces caveolin‑1 degradation and impaired mitochondrial function in E11 podocytes. Molecular Medicine Reports, 16, 7841-7847. https://doi.org/10.3892/mmr.2017.7497
MLA
Chen, Y., Lin, W., Liu, C., Su, S."H2O2 induces caveolin‑1 degradation and impaired mitochondrial function in E11 podocytes". Molecular Medicine Reports 16.5 (2017): 7841-7847.
Chicago
Chen, Y., Lin, W., Liu, C., Su, S."H2O2 induces caveolin‑1 degradation and impaired mitochondrial function in E11 podocytes". Molecular Medicine Reports 16, no. 5 (2017): 7841-7847. https://doi.org/10.3892/mmr.2017.7497