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Isolating, Sequencing and Analyzing Extracellular MicroRNAs from Human Mesenchymal Stem Cells
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Isolating, Sequencing and Analyzing Extracellular MicroRNAs from Human Mesenchymal Stem Cells

Published on: March 8, 2019

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MicroRNA-141-3p plays a role in human mesenchymal stem cell aging by directly targeting ZMPSTE24

Kyung-Rok Yu1, Seunghee Lee, Ji-Won Jung

  • 1Adult Stem Cell Research Center, College of Veterinary Medicine, Seoul National University, Seoul, Korea.

Journal of Cell Science
|October 9, 2013
PubMed

Insights

Cellular senescence in human mesenchymal stem cells (hMSCs) is linked to prelamin A accumulation. MicroRNA-141-3p exacerbates this by downregulating ZMPSTE24, impacting MSC aging.

Area of Science:

  • Cellular and Molecular Biology
  • Stem Cell Biology
  • Gerontology

Background:

  • Human mesenchymal stem cell (hMSC) aging impairs tissue regeneration and physiological functions.
  • The precise molecular mechanisms driving hMSC aging, particularly concerning prelamin A accumulation, remain unclear.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying hMSC aging driven by prelamin A accumulation.
  • To identify key regulators involved in prelamin A accumulation and its downstream effects in hMSCs.

Main Methods:

  • Investigated prelamin A accumulation in the nuclear envelope of senescent hMSCs.
  • Utilized 3'UTR-luciferase reporter assays to confirm direct binding of miR-141-3p to ZMPSTE24 transcripts.
  • Analyzed the role of ZMPSTE24 in post-translational maturation of lamin A and its relation to senescence.

Main Results:

  • Prelamin A accumulation in the nuclear envelope induces cellular senescence in hMSCs.
  • ZMPSTE24, crucial for lamin A maturation, was identified as a primary contributor to prelamin A accumulation during hMSC senescence.
  • miR-141-3p directly binds to ZMPSTE24, decreasing its expression and consequently upregulating prelamin A levels in hMSCs.
  • miR-141-3p is epigenetically regulated and overexpressed in senescent cells.

Conclusions:

  • This study reveals that miR-141-3p-mediated downregulation of ZMPSTE24 is a key mechanism driving prelamin A accumulation and subsequent senescence in hMSCs.
  • Findings offer novel insights into the regulation of MSC aging and suggest potential therapeutic targets for mitigating age-associated MSC pool depletion.
Keywords:
AgingHistone modificationMesenchymal stem cellsPrelamin A accumulationZMPSTE24miRNA-141-3p

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