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Knockdown of SMYD3 by RNA Interference Regulates the Expression of Autophagy-Related Proteins and Inhibits Bone

Jie Deng1,2, Xiaoxiao Zeng1,2, Kailin Zhang1,3

  • 1Key Laboratory of Endemic and Ethnic Diseases of the Ministry of Education, Guiyang, 550004, Guizhou, China.

Biological Trace Element Research
|August 6, 2024
PubMed

Insights

Fluoride exposure disrupts bone metabolism, increasing OC and BALP levels. Silencing SMYD3 (SET and MYND domain containing 3) reduces these markers by inhibiting fluoride-induced autophagy.

Area of Science:

  • Bone Biology and Metabolism
  • Environmental Toxicology
  • Cellular Mechanisms

Background:

  • Skeletal fluorosis, often linked to coal-burning pollution, causes orthopedic issues.
  • Fluoride exposure impacts bone metabolism, but the underlying cellular mechanisms require further elucidation.
  • The role of histone methyltransferase SMYD3 (SET and MYND domain containing 3) in fluoride-induced bone alterations is not well understood.

Purpose of the Study:

  • To investigate the role of SMYD3 in osteoblast response to fluoride exposure.
  • To determine the relationship between SMYD3, bone metabolism markers (OC, BALP), autophagy, and the Wnt/β-catenin pathway in skeletal fluorosis.
  • To explore SMYD3 as a potential therapeutic target for fluoride-induced bone abnormalities.

Main Methods:

  • Analysis of urine fluoride, BALP, OC, and SMYD3 mRNA in skeletal fluorosis patients and controls.
  • In vitro studies using human osteoblast-like MG63 cells and rat primary osteoblasts treated with sodium fluoride (NaF).
  • Assessment of SMYD3 protein expression, OC content, BALP activity, autophagosome formation, and Wnt/β-catenin pathway components following SMYD3 knockdown.

Main Results:

  • Skeletal fluorosis patients showed elevated OC and BALP but decreased SMYD3 mRNA.
  • NaF treatment in osteoblasts increased OC, BALP, SMYD3 expression, and induced autophagosome formation.
  • SMYD3 knockdown significantly reduced OC and BALP levels and inhibited fluoride-induced autophagy, without affecting the Wnt/β-catenin pathway.

Conclusions:

  • Fluoride exposure impairs bone metabolism and normal bone formation.
  • SMYD3 plays a crucial role in mediating fluoride-induced osteoblast responses, primarily through autophagy.
  • Targeting SMYD3 may offer a strategy to mitigate fluoride-induced bone damage by modulating autophagy.
Keywords:
Alkaline phosphataseAutophagyOsteoblastOsteocalcinSET and MYND domain containing 3Wnt/β-catenin pathway

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