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Reversion of glucocorticoid-induced senescence and collagen synthesis decrease by LY294002 is mediated through p38 in

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Glucocorticoids cause skin atrophy by suppressing collagen. LY294002 (LY) protects against this by activating p38 signaling, reversing atrophy markers and collagen loss without inhibiting anti-inflammatory effects.

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LY294002clobetasol propionatedermal fibroblastsglucocorticoidp38 MAPKskin atrophy

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Area of Science:

  • Dermatology and Molecular Biology
  • Investigating the molecular mechanisms of skin aging and therapeutic interventions.

Background:

  • Glucocorticoids (GCs) are primary treatments for inflammatory skin conditions but cause adverse effects like atrophy and collagen reduction.
  • The active glucocorticoid receptor (GR) suppresses collagen synthesis via transcription factors and p38 signaling.
  • LY294002 (LY), a PI3K inhibitor, shows epidermal protection against GCs, but its dermal effects are unknown.

Purpose of the Study:

  • To investigate the protective effects of LY294002 (LY) against clobetasol propionate (CP)-induced dermal atrophy in human dermal fibroblasts and mice.
  • To elucidate the role of p38 signaling in LY's protective mechanism against GC-induced skin aging.

Main Methods:

  • Dermal atrophy was modeled using clobetasol propionate (CP) in human dermal fibroblasts (HDFs) and C57BL/6 mice.
  • Key markers including FKBP51, phosphorylated GR, fibroblast proliferation, and collagen synthesis were measured.
  • The effect of LY294002 (LY) and its interaction with p38 inhibitors were analyzed.

Main Results:

  • CP significantly upregulated the atrophy marker FKBP51 and phosphorylated GR, decreased fibroblast proliferation, and reduced collagen synthesis.
  • LY treatment reversed these CP-induced changes, mitigating dermal atrophy and aging without inhibiting cell growth.
  • LY's protective effect was dose-dependently reversed by p38 inhibition, indicating p38 activation is crucial for LY's action.

Conclusions:

  • LY294002 mitigates glucocorticoid-induced dermal atrophy by activating p38 signaling, which counteracts FKBP51 upregulation and GR phosphorylation.
  • This mechanism preserves collagen synthesis and fibroblast proliferation while maintaining the anti-inflammatory properties of glucocorticoids.
  • LY represents a potential therapeutic strategy to prevent or treat glucocorticoid-induced skin atrophy.