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Nuclear factor I-C disrupts cellular homeostasis between autophagy and apoptosis via miR-200b-Ambra1 in neural tube

Wanqi Huang1, Tianchu Huang1, Yusi Liu1

  • 1Key Laboratory of Health Ministry for Congenital Malformation, Shengjing Hospital, China Medical University, Shenyang, China.

Cell Death & Disease
|December 21, 2021
PubMed

Insights

Nuclear factor I-C (NFIC) disruption of cellular homeostasis contributes to neural tube defects (NTDs). The NFIC-miR-200b-Ambra1 pathway highlights a novel mechanism in NTD pathogenesis.

Area of Science:

  • Developmental Biology
  • Cellular Biology
  • Genetics

Background:

  • Neural tube defects (NTDs) result from impaired cellular homeostasis due to disrupted autophagy and excessive apoptosis.
  • The precise regulatory mechanisms driving NTD development remain largely unknown.

Purpose of the Study:

  • To investigate the role of the transcription factor nuclear factor I-C (NFIC) in maintaining cellular homeostasis within the context of NTDs.
  • To elucidate the molecular pathway involving NFIC, miR-200b, and Ambra1 in NTD pathogenesis.

Main Methods:

  • Utilized a mouse model of NTDs to study NFIC levels and function.
  • Analyzed the interaction between NFIC and the miR-200b promoter.
  • Investigated the regulatory effects of miR-200b on autophagy and apoptosis via Ambra1.
  • Assessed the impact of miR-200b inhibitors on cellular processes.

Main Results:

  • Abnormally elevated NFIC levels were observed in the NTD mouse model.
  • NFIC directly interacts with the miR-200b promoter, increasing miR-200b transcription.
  • miR-200b represses autophagy and promotes apoptosis by targeting the autophagy-related gene Ambra1.
  • Inhibition of miR-200b reversed the detrimental effects of NFIC on autophagy and apoptosis.

Conclusions:

  • The NFIC-miR-200b-Ambra1 axis disrupts cellular homeostasis during neural tube closure.
  • This pathway, integrating transcription factors, miRNAs, and autophagy regulators, offers new insights into NTD pathogenesis.
  • Targeting this axis may present novel therapeutic strategies for NTDs.

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