Autophagy-disrupted LC3 abundance leads to death of supporting cells of human oocytes

Woojin Kang, Eri Ishida, Kenji Yamatoya, Akihiro Nakamura, Mami Miyado, Yoshitaka Miyamoto, Maki Iwai, Kuniko Tatsumi, Takakazu Saito, Kazuki Saito, Natsuko Kawano, Toshio Hamatani, Akihiro Umezawa, Kenji Miyado, Hidekazu Saito

Research output: Contribution to journalArticlepeer-review

13 Citations (Scopus)


Autophagic recycling of cell parts is generally termed as the opposite of cell death. Here, we explored the relation between cell death and autophagy by examining granulosa cell layers that control oocyte quality, which is important for the success of fertilization. Granulosa cell layers were collected from infertile women and morphologically divided into four types, viz., mature (MCCs), immature (ICCs), and dysmature cumulus cells (DCCs), and mural granulosa cells (MGCs). Microtubule-associated protein light chain 3 (LC3), which is involved in autophagosome formation, was expressed excessively in DCCs and MGCs, and their chromosomal DNA was highly fragmented. However, autophagy initiation was limited to MGCs, as indicated by the expression of membrane-bound LC3-II and autophagy-related protein 7 (ATG7), an enzyme that converts LC3-I to LC3-II. Although pro-LC3 was accumulated, autophagy was disabled in DCCs, resulting in cell death. Our results suggest the possibility that autophagy-independent accumulation of pro-LC3 proteins leads to the death of human granulosa cells surrounding the oocytes and presumably reduces oocyte quality and female fertility.

Original languageEnglish
Pages (from-to)107-114
Number of pages8
JournalBiochemistry and Biophysics Reports
Publication statusPublished - 2018 Sept


  • ATG7
  • Autophagy
  • Cell death
  • Cumulus cells
  • Human granulosa cells
  • LC3

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry


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