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Autophagy activation is required for homocysteine-induced apoptosis in bovine aorta endothelial cells

Keisuke Sato1, Tomonari Nishii1, Ayana Sato1

  • 1Department of Pharmacy, Hokkaido University of Science, 7-15-4-1 Maeda, Teine, Sapporo, Hokkaido, 006-8585, Japan.

Heliyon
|February 6, 2020
PubMed

Insights

Autophagy activation by amino acid starvation worsens homocysteine (Hcy)-induced cell death in bovine aorta endothelial cells (BAECs). An SLC7A11 inhibitor, SASP, protected against this Hcy-induced apoptosis, revealing a potential therapeutic target.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Cardiovascular Research

Background:

  • Elevated plasma homocysteine (Hcy) is a risk factor for cardiovascular and central nervous system diseases.
  • Endothelial dysfunction, driven by endothelial cell apoptosis, contributes to disease development.

Purpose of the Study:

  • To investigate the impact of autophagy activation via amino acid starvation on Hcy-induced cytotoxicity in bovine aorta endothelial cells (BAECs).

Main Methods:

  • Induction of autophagy through amino acid starvation in BAECs.
  • Assessment of Hcy-induced lactate dehydrogenase (LDH) release and cleaved caspase-3 levels.
  • Evaluation of the protective effect of Salazosulfapyridine (SASP), an SLC7A11 inhibitor.

Main Results:

  • Amino acid starvation enhanced Hcy-induced LDH release and apoptosis (cleaved caspase-3 levels) in BAECs.
  • Oxidative stress was not implicated in Hcy-induced cytotoxicity under these conditions.
  • SASP treatment mitigated Hcy-induced LDH release and apoptosis, indicating SLC7A11's role.

Conclusions:

  • Autophagy activation by amino acid starvation exacerbates Hcy-induced apoptosis in BAECs.
  • Inhibition of SLC7A11 with SASP offers protection against Hcy-induced apoptosis mediated by autophagy.

Keywords:
AntioxidantApoptosisAutophagyBiochemistryBiological sciencesBovine aorta endothelial cellCell biologyCell deathCytotoxicityHomocysteineOxidative stressSLC7A11Toxicology

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