Frontiers in Neuroscience (Jan 2021)

SPARC Knockdown Reduces Glutamate-Induced HT22 Hippocampal Nerve Cell Damage by Regulating Autophagy

  • Shuang Chen,
  • Shuang Chen,
  • Qin Zou,
  • Qiang Guo,
  • Yongmin Chen,
  • Yongmin Chen,
  • Xi Kuang,
  • Xi Kuang,
  • Yukang Zhang,
  • Yukang Zhang,
  • Yan Liu,
  • Yan Liu,
  • Wengang Wu,
  • Wengang Wu,
  • Ge Li,
  • Ge Li,
  • Linzhi Tu,
  • Linzhi Tu,
  • Jingyi Tong,
  • Jingyi Tong,
  • Songrong Li,
  • Songrong Li,
  • Lin Ma,
  • Lin Ma,
  • Qifu Li,
  • Qifu Li

DOI
https://doi.org/10.3389/fnins.2020.581441
Journal volume & issue
Vol. 14

Abstract

Read online

Secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein involved in the extracellular matrix and interactions between cells during neural development of the central nervous system (CNS). Oxidative glutamate toxicity is involved in CNS diseases, including epilepsy, Alzheimer’s disease, and ischemic stroke. However, the molecular mechanism of nerve injury is not fully understood in CNS diseases. Herein, the glutamate-induced nerve damage model was used to explore the molecular mechanisms affecting nerve damage. The levels of SPARC and autophagy were increased in glutamate-induced HT22 hippocampal nerve injury. In summary, the current study confirmed that SPARC regulates autophagy in HT22 hippocampal nerve cells, and its knockdown reduces the glutamate-induced HT22 hippocampal nerve injury by inhibiting autophagy. These findings suggested that SPARC plays a crucial role in nerve injury of CNS diseases.

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