Abstract:
Objective To investigate the effects of carboxyl terminus of Hsc70-interacting protein (CHIP) and hot shock protein 70 (Hsp70) on aluminum trichloride induced abnormal phosphorylation of tau protein in mouse neuroblastoma N2a cells.
Methods N2a cells were cultured with low, middle, and high doses of aluminium trichloride (0.5, 1.0, and 2.0 mmol/L, respectively), and the control group was treated without aluminium trichloride. The cell morphological changes were observed after 48 h of exposure under microscope and the cell viability was measured by CCK-8 assay. The protein expression levels of tau-5, pThr181, pThr231, pSer262, pSer396, CHIP, and Hsp70 were measured by Western blot.
Results As the aluminum trichloride concentration increased, the count of N2a cells decreased, the synapses retracted, and the cell body rounded. The middle and high dose groups showed significantly lower cell viabilities(91.37±0.03)% and (78.45±0.10)% than the control group(100.00±0.00)% (P < 0.05, P < 0.01). The expression level of tau-5 protein of the high dose group was significantly higher than that of the control group (P < 0.01); the expression levels of pThr231 of the middle and high dose groups were significantly higher than that of the control group (P < 0.01); the expression levels of pSer396 were higher in all aluminum trichloride groups than in the control group (P < 0.05 or P < 0.01); but no differences were found in the expression levels of pThr181 and pSer262 (P > 0.05). The expression levels of CHIP and Hsp70 of all aluminium trichloride groups were significantly higher than those of the control group (P < 0.05 or P < 0.01).
Conclusion Aluminum trichloride could increase the expression levels of pThr231 and pSer396 in N2a cells, which is possibly related to the expression changes of CHIP and Hsp70.
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