Abstract:

BACKGROUND: Many scholars believe that β-amyloid protein is the initial factor for the occurrence of Alzheimer’s disease, and the hyperphosphorylation of Tau protein may be one of the most important molecular pathological changes in Alzheimer’s disease.
OBJECTIVE: To study the effect of β-amyloid 25-35 (Aβ25-35) on Tau protein phosphorylation of rat bone marrow mesenchymal stem cells (BMSCs) differentiating into neuron-like cells.
METHODS: BMSCs were isolated and purified from SD rats, and the fourth passage BMSCs were divided into two groups: Aβ25-35 experiment group was added pre-induction medium (containing 10 μg/L bFGF, 10% FBS in DMEM) and 20 μmol/L Aβ25-35, 24 hours later, the cells were induced into neurons-like cells by DMEM with 2% DMSO and 200 μmol/L BHA, and harvested 5 hours later; control group was treated with the same induction method but with no Aβ25-35. Morphological changes were observed by light microscope, neuron-specific enolase (NSE) detected by immunocytochemistry; GSK-3β, Tau [pSer262] and Tau [pSer396] are tested by Western blot.
RESULTS AND CONCLUSION: With the observation of light microscope, spindle shaped BMSCs after induction showed up neuron-like cells shape with long projections, which were different from Aβ25-35 experiment group with the length and quantity of the projections shorter and less; both two groups showed Tau+ by immunocytochemistry; Western blotting showed that GSK-3β, Tau [pSer262] and Tau [pSer396] of Aβ25-35 treatment group were significantly higher than those of the control group. Aβ25-35 can induce BMSCs differentiating into neuron-like cells leading to the hyperphosphorylation of Tau protein through GSK-3.