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Sodium fluoride induces apoptosis and autophagy via the endoplasmic reticulum stress pathway in MC3T3-E1 osteoblastic

Xueyan Li1, Li Meng2, Feng Wang3

  • 1Department of Stomatology, Eye & Ent Hospital of Fudan University, Shanghai, 200031, China.

Molecular and Cellular Biochemistry
|December 7, 2018
PubMed

Insights

Excessive fluoride intake, specifically sodium fluoride (NaF), inhibits osteoblast proliferation and induces cell death through endoplasmic reticulum (ER) stress, unfolded protein response (UPR), and autophagy.

Area of Science:

  • Cell Biology
  • Toxicology
  • Biochemistry

Background:

  • Chronic or excessive fluoride intake is linked to fluorosis and bone pathologies.
  • Limited research exists on the cellular mechanisms of osteoblast toxicity from sodium fluoride (NaF).

Purpose of the Study:

  • To investigate the effects of NaF on MC3T3-E1 osteoblast cells.
  • To elucidate the cellular pathways involved in NaF-induced osteoblast toxicity.

Main Methods:

  • Exposure of MC3T3-E1 cells to NaF.
  • Assessment of cell proliferation and apoptosis.
  • Analysis of endoplasmic reticulum (ER) stress markers, including unfolded protein response (UPR) proteins (GRP94, BiP), and caspase-associated proteins.
  • Investigation of autophagy pathways.

Main Results:

  • NaF significantly inhibited MC3T3-E1 cell proliferation.
  • NaF induced apoptosis, evidenced by increased caspase expression and apoptotic body formation.
  • NaF triggered ER stress, activating the UPR and upregulating GRP94 and BiP.
  • ER stress was identified as a key mediator in NaF-induced autophagy and apoptosis.
  • Inhibition of NaF-induced autophagy promoted apoptosis.

Conclusions:

  • NaF exposure activates the ER stress-signaling pathway in osteoblasts.
  • This activation leads to increased autophagy and apoptosis, impacting cell proliferation and survival.
  • ER stress is a critical factor in NaF-induced osteoblast toxicity.
Keywords:
ApoptosisAutophagyER stressOsteoblastic cellsSodium fluoride

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