Inhibition of BAG‐1 induced SH‐SY5Y cell apoptosis without affecting Hsp70 expression

Objective To further explore the role of BCL‐2 associated anthanogen‐1 (BAG‐1) in neuronal apoptosis and whether the effect of BAG‐1 depends on heat shock protein 70 (HSP70). Methods RNA interference (RNAi) technology was used to inhibit the expression of BAG‐1 in SH‐SY5Y cells. Hypoxia‐reoxygenation injury model in the SH‐SY5Y cells was established. Cell Counting Kit‐8 (CCK‐8) was performed for cell viability. Annexin V‐APC/7‐AAD double‐staining followed by flow cytometry was used to measure cell apoptosis. Quantitative reverse‐transcription polymerase chain reaction and Western blot analysis were used to detect the messenger RNA (mRNA) and protein expression of genes, respectively. Results BAG‐1 gene silencing decreased SH‐SY5Y cell viability and promoted SH‐SY5Y cell apoptosis after hypoxia‐reoxygenation. However, the down‐regulation of BAG‐1 had no effect on the mRNA and protein expression of HSP70. Conclusion BAG‐1 could protect SH‐SY5Y cells from the hypoxia‐reoxygenation injury without affecting HSP70 expression. BCL‐2 associated anthanogen‐1 (BAG‐1) is a multifunctional protein that is involved in apoptosis, proliferation, and signal transduction. However, its role in neuronal apoptosis and the underlying mechanism are still poorly understood. In this study, we found that BAG‐1 gene silencing decreased SH‐SY5Y cell viability and promoted SH‐SY5Y cell apoptosis after hypoxia‐reoxygenation. However, the downregulation of BAG‐1 had no effect on the messenger RNA and protein expression of HSP70. Therefore, BAG‐1 could protect SH‐SY5Y cells from the hypoxia‐reoxygenation injury without affecting HSP70 expression. These results provided theoretical basis for the development of new drugs and treatments for cerebrovascular disease.