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Stimulation of Stem Cell Niches and Tissue Regeneration in Mouse Skin by Switchable Protoporphyrin IX-Dependent Photogeneration of Reactive Oxygen Species In Situ
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MiR-30a-5p Alters Epidermal Terminal Differentiation during Aging by Regulating BNIP3L/NIX-Dependent Mitophagy

Fabien P Chevalier1,2, Julie Rorteau1,3, Sandra Ferraro1

  • 1CNRS UMR 5305, Tissue Biology and Therapeutic Engineering Laboratory (LBTI), 69007 Lyon, France.

Cells
|March 10, 2022
PubMed

Insights

Aging impairs skin function as epidermal keratinocytes fail to differentiate. MicroRNA-30a (miR-30a) overexpression reduces mitophagy receptor BNIP3L, hindering mitochondrial clearance and epidermal homeostasis in aging skin.

Area of Science:

  • Cellular and Molecular Biology
  • Dermatology
  • Aging Research

Background:

  • Chronological aging alters gene regulatory networks, impacting skin function.
  • Epidermal keratinocyte differentiation declines with age, weakening the skin barrier.
  • MicroRNA-30a (miR-30a) is overexpressed in aging epidermis, but its role is unclear.

Purpose of the Study:

  • To investigate the effects of miR-30a overexpression on human epidermal keratinocyte differentiation.
  • To identify downstream molecular targets of miR-30a in the aging epidermis.

Main Methods:

  • Utilized a 3D organotypic model of reconstructed human epidermis overexpressing miR-30a.
  • Analyzed human epidermal skin biopsies from donors of varying ages.
  • Studied primary human keratinocytes undergoing in vitro differentiation.
  • Assessed mitophagy receptor BNIP3L expression and mitochondrial metabolism (ATP-linked respiration).

Main Results:

  • Identified BNIP3L as a direct target of miR-30a.
  • Observed reduced BNIP3L expression in the granular layer of miR-30a overexpressing epidermis and in aged skin.
  • Found decreased BNIP3L expression and mitochondrial retention in aging primary keratinocytes during differentiation.
  • Detected altered mitochondrial metabolism, including decreased ATP-linked respiration, in aging keratinocytes.

Conclusions:

  • miR-30a negatively regulates programmed mitophagy during keratinocyte terminal differentiation.
  • Overexpression of miR-30a impairs epidermal homeostasis by inhibiting mitophagy in aging skin.
  • This mechanism contributes to the functional decline of the epidermis associated with chronological aging.
Keywords:
BNIP3LagingkeratinocytemiR-30amitochondriamitophagy

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