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Inhibitory Effects of Sulfur Dioxide on Rat Myocardial Fibroblast Proliferation and Migration

Lu-Lu Zhang1, Jun-Bao Du2, Chao-Shu Tang3

  • 1Department of Pediatrics, Peking University First Hospital, Beijing 100034, China.

Chinese Medical Journal
|July 13, 2018
PubMed
Abstract

Insights

Endogenous sulfur dioxide (SO2) inhibits myocardial fibroblast proliferation and migration by suppressing the ERK signaling pathway. This finding suggests SO2 as a potential therapeutic target for heart diseases involving fibrosis.

Area of Science:

  • Cardiovascular Biology
  • Cellular Physiology
  • Biochemistry

Background:

  • Myocardial fibrosis is a critical pathological process in various heart conditions, yet its underlying mechanisms remain incompletely understood.
  • Investigating novel endogenous regulators of myocardial fibroblast behavior is crucial for developing targeted therapies.

Purpose of the Study:

  • To determine if endogenous sulfur dioxide (SO2) acts as an inhibitor of myocardial fibroblast proliferation and migration.
  • To elucidate the molecular mechanisms by which SO2 influences fibroblast activity.

Main Methods:

  • Primary rat myocardial fibroblasts were utilized, with knockdown of aspartate aminotransferase (AAT1 and AAT2) achieved via lentivirus transfection.
  • Sulfur dioxide (SO2) levels were quantified using high-performance liquid chromatography, and protein expression (AAT1, AAT2, PCNA, p-ERK, T-ERK) was assessed.
  • Cell proliferation and migration were evaluated using Cell Counting Kit-8 (CCK-8) and wound healing assays, respectively. Statistical analysis included independent sample t-tests and one-way ANOVA.

Main Results:

  • Knockdown of AAT1 and AAT2 significantly decreased endogenous SO2 levels and protein expression, while concurrently increasing fibroblast proliferation and migration.
  • Exogenous SO2 supplementation, but not pyruvate, counteracted the pro-proliferative and migratory effects induced by AAT knockdown.
  • AAT1/2 knockdown led to increased phosphorylation of extracellular signal-regulated kinase (ERK), and inhibition of ERK activation by PD98059 abrogated the enhanced proliferation and migration.

Conclusions:

  • Endogenous sulfur dioxide (SO2) functions as a novel inhibitor of myocardial fibroblast proliferation and migration.
  • The inhibitory effect of SO2 on fibroblasts is mediated through the suppression of the ERK signaling pathway.
  • These findings highlight the potential of endogenous SO2 as a therapeutic target for mitigating myocardial fibrosis.
Keywords:
EndogenousFibroblastMigrationProliferationSulfur Dioxide

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