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2 results on '"Linzhi Tu"'

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

Author

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

Subjects
SPARC, autophagy, glutamate, HT22, epilepsy, neurological diseases, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
Abstract

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.

Published
2021
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2. HDAC9 in the Injury of Vascular Endothelial Cell Mediated by P38 MAPK Pathway

Author

Xi Kuang, Shuang Chen, Jitong Lao, Yongmin Chen, Dandan Jia, Linzhi Tu, Lin Ma, Xiaoping Liao, Wenjie Zhao, and Qifu Li

Subjects
MAP Kinase Signaling System, Immunology, Endothelial Cells, Cell Biology, p38 Mitogen-Activated Protein Kinases, Histone Deacetylases, Lipoproteins, LDL, Repressor Proteins, Gene Knockdown Techniques, Virology, Humans, Disease Susceptibility, Endothelium, Vascular, RNA, Small Interfering, Protein Kinase Inhibitors, Biomarkers, Cells, Cultured
Abstract

Ischemic stroke caused by atherosclerosis (AS) poses a serious threat to human life expectancy and quality. With the development of genome-wide association studies, the association of histone deacetylase 9 (HDAC9) expression of atheromatous plaques with ischemic stroke in large arteries has been revealed, but the molecular mechanisms behind this phenomenon have not been elucidated. In this study, we explored the effect of HDAC9 on the P38 mitogen activated protein kinase (P38 MAPK), a classic cellular inflammation-related pathway, by knocking down HDAC9 in vascular endothelial cells with short hairpin RNA (shRNA) and found that HDAC9 may mediate oxidized low density lipoprotein (ox-LDL)-induced inflammatory injury in vascular endothelial cells by regulating the phosphorylation level of P38 MAPK to lead to AS. It can be seen that HDAC9 may be a target to control the formation of atherosclerotic plaques. In follow-up experiments, it was verified that sodium valproate (SVA), as a HDAC9 inhibitor, can indeed antagonize the inflammatory damage of vascular endothelial cells, as well as SB203580, which is a P38 MAPK inhibitor. It proves that SVA may be a potential drug for the prevention and treatment of ischemic stroke.

Published
2021

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