Protective effect of bone marrow mesenchymal stem cells on PC12 cells apoptosis mediated by TAG1
Yu-Zhen Zhang1, Ji-Yu Lou1, Hong-Ying Bai1
1Department of Neurology, The Second Affiliated Hospital of Zhengzhou University Zhengzhou, P. R. China.
Objective:
This study aims to explore the protection effect of bone marrow mesenchymal stem cells (BMSCs) on PC12 cells apoptosis mediated by transient axonal glycoprotein 1 (TAG1).
Methods:
PC12 cells were divided into control group, Aβ25-35 group and BMSCs + Aβ25-35 group. The effects of BMSCs on PC12 cells treated by Aβ25-35 were detected using MTT, Hoechst 33258 and Annexin V-FITC/PI staining methods. The expression levels of TAG1, β-amyloid precursor protein (APP), AICD and p53 were determined by RT-PCR and Western blotting methods. The expression levels of Bax and Bcl-2 were determined by Western blotting method. The activity of Caspase 3 was detected by spectrophotometric method.
Results:
MTT results showed that cell activity decreased after the treatment of 20 μM Aβ25-35 for 48 h (P<0.01) while it increased in BMSCs + Aβ25-35 group (P<0.01). Hoechst 33258 and Annexin V-FITC/PI staining results showed that Aβ25-35 could induce the apoptosis of PC12 cells while the apoptosis of PC12 cells was inhibited in BMSCs + Aβ25-35 group. RT-PCR and Western blotting methods showed that 20 μM Aβ25-35 could increase the expression levels of TAG1, APP, AICD and p53 (P<0.01) while they decreased in BMSCs + Aβ25-35 group (P<0.01). 20 μM Aβ25-35 could increase the expression levels of Bax and decrease the expression levels of Bcl-2 (P<0.01), while the expression levels of Bax decreased and the expression levels of Bcl-2 increase in BMSCs + Aβ25-35 group (P<0.01). 20 μM Aβ25-35 could enhance Caspase 3 activity while it decreased in BMSCs + Aβ25-35 group (P<0.01). Conclusions BMSCs with Aβ25-35 could inhibit the apoptosis of PC12 cells, which maybe related with TAG1/APP/AICD signal pathway.
