The effect of early growth response 1 on levels of Amyloid‐β 40 peptide in U87MG cells

A recent study has shown that early growth response 1 (EGR1) plays a critical role in the β‐amyloid cascade and tau hypotheses. In addition, evidence has suggested that EGR1 can regulate levels of amyloid‐beta peptides, key molecules in the pathogenesis of Alzheimer's disease (AD). However, whether EGR1 is a deleterious or protective factor in the AD is still controversial. In this present study, we constructed an overexpression plasmid, CMV‐EGFP‐EGR1‐Kanamycin, and transfected it into U87MG cells to investigate the effects of EGR1 expression on amyloid‐β (1‐40) peptide (Aβ40) levels. U87MG cells transfected by CMV‐EGFP‐EGR1‐Kanamycin and CMV‐EGFP‐Kanamycin were assigned, respectively, to experimental and control groups. Fluorescence microscopy was used to observe transfection efficiencies of the plasmids after 6 hours. EGR1 messenger RNA levels were measured by quantitative reverse transcription polymerase chain reaction. Aβ40 secretion was analyzed by enzyme‐linked immunosorbent assay. Expression of the amyloid precursor protein, beta‐secretase enzyme, and presenilin 1 proteins were analyzed by Western blot analysis. The results showed that EGR1 overexpression increased Aβ40 secretion in vitro, possibly through increasing BACE1 expression. Based on these results, EGR1 might be a promising therapeutic target for the AD. The effects of such agents on Alzheimer's disease (AD) remain to be determined. Investigators in China showed that lanthanum chloride inhibited early growth response 1 (EGR1) expression. If EGR1 expression could be controlled, inhibitory drugs might suppress the onset and development of AD, potentially representing a new direction for AD treatment