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Nuclear envelope budding inhibition slows down progerin-induced aging process.

Xiangyang Wang1,2, Lin Ma3, Di Lu4

  • 1The Key Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, College of Life Sciences, Peking University, Beijing 100871, China.

Proceedings of the National Academy of Sciences of the United States of America
|October 1, 2024
PubMed
Summary
This summary is machine-generated.

Progerin causes Hutchinson-Gilford progeria syndrome (HGPS) by inducing nuclear envelope budding, leading to accelerated aging. A drug, chaetocin, reverses these effects and extends lifespan in HGPS models.

Keywords:
ERK1/2Hutchinson–Gilford progeria syndromeNE buddingchromatin lossprogerin

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Area of Science:

  • Cell Biology
  • Aging Research
  • Genetics

Background:

  • Hutchinson-Gilford progeria syndrome (HGPS) is a premature aging disease caused by progerin accumulation.
  • The precise mechanisms by which progerin accelerates aging remain incompletely understood.
  • Nuclear envelope (NE) integrity is crucial for cellular function and aging.

Purpose of the Study:

  • To investigate the link between progerin, nuclear envelope budding, and accelerated aging.
  • To identify potential therapeutic targets for HGPS.
  • To explore the role of specific proteins in NE stability and chromatin regulation.

Main Methods:

  • Utilized primary cells and mouse models from HGPS patients.
  • Performed ectopic expression of progerin to mimic disease phenotypes.
  • Conducted high-throughput screening to identify NE budding inhibitors.
  • Assessed chromatin loss, NE budding, and lifespan in response to interventions.

Main Results:

  • Progerin expression induces NE budding and chromatin loss, mimicking HGPS.
  • Emerin antagonizes progerin-induced NE budding.
  • Chaetocin, an NE budding inhibitor, sequesters progerin, prevents NE budding, and sustains ERK1/2 activation.
  • Chaetocin treatment ameliorates HGPS defects in cellular and animal models and extends lifespan.

Conclusions:

  • Progerin-induced NE budding is a key mechanism driving HGPS and accelerated aging.
  • Chaetocin and sustained ERK1/2 activation represent promising therapeutic strategies for HGPS.
  • Targeting NE budding offers a novel therapeutic avenue for treating HGPS and potentially other aging-related diseases.