STX17 improves Aβ31-35 induced death of hippocampal neurons in mice

Abstract

Objective To explore the role of STX17 protein in Aβ-induced death of mouse hippocampal neuronal cells. Methods Based on Weighted correlation network analysis (WGCNA), the modules significantly related to Alzheimer's disease (AD) were selected, and key genes were screened for cross-fertilization with autophagy gene bank and SNARE family genes. Aβ31-35 at a concentration of 1 g/L was used to inject the C57BL/6 mouse hippocampal tissue, and HT22 hippocampal neuronal cells were treated with 5 μmol/L Aβ31-35. Then the protein expression of STX17, LC3 Ⅱ and P62 was detected by Western blotting. The survival rate of the HT22 hippocampal neuronal cells treated by using Aβ31-35 was detected by CCK-8 assay. Protein expression of LC3Ⅱ and P62 were determined by Western blotting after overexpression STX17 in HT22 hippocampal neuronal cells. Results The Salmon and Black modules significantly associated with AD crossed with autophagic gene pool and SNARE subfamily intersection STX17, respectively. Under the action of Aβ31-35 mouse hippocampal tissue and mouse HT22 hippocampal neuronal cells, and the survival rate of HT22 cells [(81.81±11.65)% vs (100.00±12.89)%, P < 0.05] were decreased significantly, and the expression of STX17 was significantly reduced in both tissue and cells (P < 0.05). The expression of tissue LC3Ⅱ and P62 proteins were significantly elevated in the tissue (P < 0.05), and in the cells (P < 0.05). After lentivirus-mediated overexpression of STX17 in HT22 hippocampal neuronal cells, the protein expression upregulation of LC3II and P62 induced by Aβ31-35 was significantly reversed, and the survival rate was improved in Aβ31-35-induced HT22 hippocampal neuronal cells [(101.91±13.81)% vs (79.21±8.75)%, P < 0.05]. Conclusion STX17 improves Aβ-induced death of mouse hippocampal neuronal cells by promoting autophagy.

Keywords

• stx17 protein
• aβ
• mouse hippocampal neuronal cells
• cell death
• autophagy