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ABSTRACT
Objective
EGR1 has been implicated in the progression of spinal cord injury (SCI). Nevertheless, its specific mechanism in SCI remains to be investigated. Hence, this study explored the potential mechanism of EGR1 in SCI by focusing on neuron apoptosis.
Methods
H2O2 was utilized to treat rat neurons-dorsal spinal cord (RN-dsc) for the construction of an in vitro model of SCI. Afterwards, cell survival, apoptosis, and LDH leakage were detected to evaluate the injury degree of H2O2-treated RN-dsc. The expression of apoptosis-related proteins was also measured. Additionally, EGR1 was silenced and/or BTG2 was overexpressed in RN-dsc before H2O2 treatment to assess the impacts of EGR1 and BTG2 on H2O2-induced RN-dsc. Jasper online website was utilized to predict binding sites of EGR1 on BTG2, and dual-luciferase reporter gene and chromatin immunoprecipitation (ChIP) assays were utilized to verify the binding between EGR1 and BTG2.
Results
H2O2 treatment suppressed survival and promoted apoptosis in RN-dsc, accompanied by upregulated LDH, Bax, and cleaved-caspase-3 and down-regulated Bcl-2. Moreover, EGR1 and BTG2 were up-regulated in H2O2-induced RN-dsc. Mechanistically, EGR1 was bound to the promoter of BTG2 to transcriptionally activate BTG2. EGR1 knockdown diminished apoptosis and LDH, Bax, and cleaved-caspase-3 levels while elevating survival and Bcl-2 levels in H2O2-induced RN-dsc. These effects of EGR1 knockdown were abrogated by further BTG2 overexpression.
Discussion
Conclusively, EGR1 promotes H2O2-induced apoptosis in RN-dsc by activating BTG2 transcription.
Disclosure statement
The authors report no relationships that could be construed as a conflict of interest.