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Phospholipid peroxidation-driven modification of chondrogenic transcription factor mediates alkoxyl radicals-induced

Jie Niu1, Xin Wan2, Gui-Yuan Yu3

  • 1Guangdong Engineering Research Center of Chinese Medicine & Disease Susceptibility, Jinan University, Guangzhou, 510632, China; International Cooperative Laboratory of Traditional Chinese Medicine Modernization and Innovative Drug Development of Chinese Ministry of Education (MOE), Jinan University, Guangzhou, 510632, China; Guangdong Province Key Laboratory of Pharmacodynamic Constituents of TCM and New Drugs Research, Jinan University, Guangzhou, 510632, China; Joint Laboratory of Dalian Runsheng Kangtai and Jinan University, Jinan University, China.

Redox Biology
|August 29, 2022
PubMed

Insights

Maternal stress causes abnormal fetal bone development via alkoxyl radicals and phospholipid peroxidation. Targeting this process may treat related bone disorders.

Area of Science:

  • Developmental Biology
  • Toxicology
  • Biochemistry

Background:

  • Maternal stress is linked to adverse birth outcomes.
  • Oxidative stress is implicated in embryonic bone development disorders.
  • Free radicals, like alkoxyl radicals, may contribute to these issues.

Purpose of the Study:

  • To investigate the role of alkoxyl radicals in fetal bone development.
  • To elucidate the mechanism linking maternal stress, oxidative stress, and bone abnormalities.
  • To identify potential therapeutic targets for related disorders.

Main Methods:

  • Utilized alkoxyl radical generators to induce effects in embryonic models.
  • Analyzed chondrocyte ferroptosis and phospholipid oxidation.
  • Investigated the interaction of 4-hydroxynonenal (4-HNE) with SOX9 transcription factor.

Main Results:

  • Alkoxyl radicals induced prenatal bone growth retardation and chondrocyte ferroptosis.
  • Accumulation of oxidized phospholipids in chondrocytes was observed via iron-mediated Fenton reaction.
  • 4-HNE adduct formation with SOX9 led to its degradation, inhibiting chondrogenesis.

Conclusions:

  • Phospholipid peroxidation is critical in alkoxyl radical-induced abnormal chondrogenesis.
  • Alkoxyl radicals disrupt fetal bone development through SOX9 degradation.
  • This pathway presents a target for treating oxidative stress-related bone disorders.

Keywords:
Alkoxyl radicalsChondrogenesisChondrogenic transcription factorEmbryonic bone developmentFerroptosisLipid peroxidation

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