Enhanced Mitophagy in Cholesteatoma Epithelial Cells.

Otol Neurotol

Department of Otolaryngology-Head and Neck Surgery, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.

Published: October 2023

AI Article Synopsis

  • The study explores the role of mitophagy in acquired cholesteatoma, a condition that shows characteristics similar to cancer.
  • Researchers analyzed specific autophagy and mitophagy protein markers in cholesteatoma epithelial cells compared to normal ear canal cells using various methods, including immunoblotting and electron microscopy.
  • Results indicated increased mitophagy activity in cholesteatoma cells, suggesting that this process may contribute to the development of cholesteatoma.

Article Abstract

Hypothesis: Mitophagy may have a potential role in the pathogenesis of acquired cholesteatoma.

Background: Enhanced mitophagy has been proven to be involved in various cancers. However, its role in the pathogenesis of cholesteatoma, which shares some common features with cancer, is controversial. This study investigated mitophagy in cholesteatoma epithelial cells.

Methods: The autophagy protein markers LC3-II and p62 and mitophagy proteins BNIP3, Parkin, and PINK1 were analyzed in cholesteatoma epithelial cells and external auditory canal epithelium cells by immunoblotting. The results were confirmed by immunohistochemistry. Adenovirus Ad-mCherry-GFP-LC3B and Ad-GFP-LC3B were used to evaluate autophagic activity. Transmission electron microscopy was used to observe and analyze autophagosomes.

Results: LC3-II expression was increased in cholesteatoma cells, whereas soluble and insoluble p62 levels were decreased. The expressions of BNIP3, Parkin, and PINK1 were higher in total protein and mitochondrial protein of cholesteatoma cells compared with normal external auditory canal epithelium cells. Autophagic activity was increased in cholesteatoma cells compared with normal external auditory canal epithelium cells.

Conclusion: Mitophagy was enhanced in cholesteatoma epithelial cells and may have a potential role in the pathogenesis of acquired cholesteatoma.

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Source
http://dx.doi.org/10.1097/MAO.0000000000003986DOI Listing

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