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MicroRNA-212-5p Prevents Dopaminergic Neuron Death by Inhibiting SIRT2 in MPTP-Induced Mouse Model of Parkinson’s Disease

Sun, Sifan, Han, Xiaojuan, Li, Xueting, Song, Qiqi, Lu, Ming, Jia, Miaomiao, Ding, Jianhua, Hu, Gang·2018·Frontiers in Molecular Neuroscience
DOI 10.3389/fnmol.2018.00381PMC PMC6193094
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FIGURE 1 The expression patterns of SIRT2 in PD model. (A–D) Western blotting analysis showed that SIRT2 protein level increased by MPTP treatment or MPP+ stimulating, respectively. (E) Immunohistochemistry staining showed a significant increment of SIRT2 in SH-SY5Y cells by MPP+ stimulation, compared with controls. Scale bar: 40 μm. (F,G) Quantitative RT-PCR analysis for SIRT2 mRNA level showed no significant difference in midbrain tissues and SH-SY5Y cells under treatment. Data are presented as the mean ± SEM for each group of five mice or three independent in vitro experiments. ∗p < 0.05, ∗∗p < 0.01 versus corresponding control group.
FIGURE 1 The expression patterns of SIRT2 in PD model. (A–D) Western blotting analysis showed that SIRT2 protein level increased by MPTP treatment or MPP+ stimulating, respectively. (E) Immunohistochemistry staining showed a significant increment of SIRT2 in SH-SY5Y cells by MPP+ stimulation, compared with controls. Scale bar: 40 μm. (F,G) Quantitative RT-PCR analysis for SIRT2 mRNA level showed no significant difference in midbrain tissues and SH-SY5Y cells under treatment. Data are presented as the mean ± SEM for each group of five mice or three independent in vitro experiments. ∗p < 0.05, ∗∗p < 0.01 versus corresponding control group.CC BY · PubMed Central
FIGURE 2 SIRT2 is a target gene of miR-212-5p. (A,B) Quantitative RT-PCR analysis detected some predicted SIRT2-associated microRNAs expression. Results showed miR-212-5p significantly decreased in PD model both in vivo and in vitro. (C) The predicted binding sites of miR-212-5p in the 3′UTR of SIRT2, and schematic description of the base-pairing interaction between miR-212-5p and SIRT2 mRNA. (D) Luciferase reporter assays confirm that SIRT2 is a direct target gene of miR-212-5p in HEK293T cells. (E–G) Transfection of miR-212-5p into SH-SY5Y cells significantly reduced SIRT2 expression but failed to affect SIRT1 expression. (H–J) Anti-miR-212-5p up-regulated SIRT2 expression without significant difference, but had no effect on SIRT1 expression. Data are presented as the mean ± SEM from three independent experiments. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 versus control or NC-control group; #p < 0.05 versus NC plus MPP+ group. NC, negative control.
FIGURE 2 SIRT2 is a target gene of miR-212-5p. (A,B) Quantitative RT-PCR analysis detected some predicted SIRT2-associated microRNAs expression. Results showed miR-212-5p significantly decreased in PD model both in vivo and in vitro. (C) The predicted binding sites of miR-212-5p in the 3′UTR of SIRT2, and schematic description of the base-pairing interaction between miR-212-5p and SIRT2 mRNA. (D) Luciferase reporter assays confirm that SIRT2 is a direct target gene of miR-212-5p in HEK293T cells. (E–G) Transfection of miR-212-5p into SH-SY5Y cells significantly reduced SIRT2 expression but failed to affect SIRT1 expression. (H–J) Anti-miR-212-5p up-regulated SIRT2 expression without significant difference, but had no effect on SIRT1 expression. Data are presented as the mean ± SEM from three independent experiments. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 versus control or NC-control group; #p < 0.05 versus NC plus MPP+ group. NC, negative control.CC BY · PubMed Central
FIGURE 3 MiR-212-5p promotes autophagy and inhibits apoptosis in SH-SY5Y cells. (A–C) Western blotting and quantitative analysis of LC3B and P62 revealed that transfection of miR-212-5p into SH-SY5Y cells activated autophagy. (D–F) In contrast, miR-212-5p inhibitor indeed blocked autophagy, which showed by Western blotting and quantitative analysis of autophagy markers. (G) Double immunofluorescence of GFP-LC3B (Green) and RFP-LC3B (Red). MPP+ blocked the autophagy flux in SH-SY5Y cells, which was reversed by miR-212-5p transfection. Scar bar: 40 μm. (H–J) Transfection of miR-212-5p into SH-SY5Y cells reduced apoptosis, Western blotting and quantitative analysis of cleaved caspase-3, Bcl2 and BAX. (K,L) Apoptotic cells were stained by Hoechst 33342 and analysis of positive cells. Scale bar: 80 μm. Data is presented as the mean ± SEM from three independent experiments. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 versus control or NC-control group; #p < 0.05, ##p < 0.01, ###p < 0.01 versus NC plus MPP+ group.
FIGURE 3 MiR-212-5p promotes autophagy and inhibits apoptosis in SH-SY5Y cells. (A–C) Western blotting and quantitative analysis of LC3B and P62 revealed that transfection of miR-212-5p into SH-SY5Y cells activated autophagy. (D–F) In contrast, miR-212-5p inhibitor indeed blocked autophagy, which showed by Western blotting and quantitative analysis of autophagy markers. (G) Double immunofluorescence of GFP-LC3B (Green) and RFP-LC3B (Red). MPP+ blocked the autophagy flux in SH-SY5Y cells, which was reversed by miR-212-5p transfection. Scar bar: 40 μm. (H–J) Transfection of miR-212-5p into SH-SY5Y cells reduced apoptosis, Western blotting and quantitative analysis of cleaved caspase-3, Bcl2 and BAX. (K,L) Apoptotic cells were stained by Hoechst 33342 and analysis of positive cells. Scale bar: 80 μm. Data is presented as the mean ± SEM from three independent experiments. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 versus control or NC-control group; #p < 0.05, ##p < 0.01, ###p < 0.01 versus NC plus MPP+ group.CC BY · PubMed Central
FIGURE 4 MiR-212-5p regulates p53 sub-localization via SIRT2 activity in PD model. (A,B) Western blotting and quantitative analysis showed that the total p53 expression was highly increased by MPP+ stimulating, which was somehow inhibited by miR-212-5p mimic treatment. (D,E) In contrast, miR-212-5p inhibitor indeed enhanced the increased total p53 expression. Since p53 is a key deacetylation substrate of SIRT2, we detected the acetylation of p53 by Western blotting. Results showed that miR-212-5p regulated the level of acetylated p53 (C,F). (G) SIRT2 activity assay revealed that miR-2125p could suppress the deacetylation potential of SIRT2. (H) Double immunofluorescence of SIRT2 (green) and p53 (red). Scale bar: 40 μm. Consistent with previous results, SIRT2 and p53 were highly increased under MPP+ treatment, which was inhibited by miR-212-5p transfection. (I–K) Western blotting and quantitative analysis showed that p53 was up-regulated both in cytoplasm and nucleus. miR-212-5p transfection suppressed the expression of p53, especially in cytoplasm. ∗p < 0.05, ∗∗p < 0.01 versus control or NC-control group; #p < 0.05, ##p < 0.01 versus NC plus MPP+ group.
FIGURE 4 MiR-212-5p regulates p53 sub-localization via SIRT2 activity in PD model. (A,B) Western blotting and quantitative analysis showed that the total p53 expression was highly increased by MPP+ stimulating, which was somehow inhibited by miR-212-5p mimic treatment. (D,E) In contrast, miR-212-5p inhibitor indeed enhanced the increased total p53 expression. Since p53 is a key deacetylation substrate of SIRT2, we detected the acetylation of p53 by Western blotting. Results showed that miR-212-5p regulated the level of acetylated p53 (C,F). (G) SIRT2 activity assay revealed that miR-2125p could suppress the deacetylation potential of SIRT2. (H) Double immunofluorescence of SIRT2 (green) and p53 (red). Scale bar: 40 μm. Consistent with previous results, SIRT2 and p53 were highly increased under MPP+ treatment, which was inhibited by miR-212-5p transfection. (I–K) Western blotting and quantitative analysis showed that p53 was up-regulated both in cytoplasm and nucleus. miR-212-5p transfection suppressed the expression of p53, especially in cytoplasm. ∗p < 0.05, ∗∗p < 0.01 versus control or NC-control group; #p < 0.05, ##p < 0.01 versus NC plus MPP+ group.CC BY · PubMed Central
FIGURE 5 P53 transfection abolished the SIRT2-related programmed cell death in SH-SY5Y cells. (A–C) According to p53 as a key transfactor dealing with the programmed cell death, to detect the realistic role of p53 regulated by SIRT2 in this study, we transfected pcDNA3.0-Flag-p53 plasmid to SH-SY5Y cells. Western blotting and quantitative analysis showed that 1 μg and 2 μg plasmid transfection highly increased the p53 expression. (D,E) CCK-8 and LDH release assay showed that 0.5 μg and 1 μg plasmid transfection had no effects on cell viability. Thus, we transfected 1 μg pcDNA3.0-Flag-p53 plasmid to SH-SY5Y cells in the further study. (F) Immunohistochemistry staining showed a significant increment of LC3 (green) under MPP+ stimulation could suppressed by miR-212-5p transfection, which was blocked by p53 overexpression. Scar bar: 40 μm. (G,H) Apoptotic cells were stained by Hoechst 33342 and analysis of positive cells. MiR-212-5p decreased the apoptotic cells by MPP+ stimulation, which was blocked by p53 overexpression. Scale bar: 80 μm. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.01 versus Mock or Mock with NC control group; ##p < 0.01 versus pcDNA3.0-Flag-p53 plasmid plus MPP+ group.
FIGURE 5 P53 transfection abolished the SIRT2-related programmed cell death in SH-SY5Y cells. (A–C) According to p53 as a key transfactor dealing with the programmed cell death, to detect the realistic role of p53 regulated by SIRT2 in this study, we transfected pcDNA3.0-Flag-p53 plasmid to SH-SY5Y cells. Western blotting and quantitative analysis showed that 1 μg and 2 μg plasmid transfection highly increased the p53 expression. (D,E) CCK-8 and LDH release assay showed that 0.5 μg and 1 μg plasmid transfection had no effects on cell viability. Thus, we transfected 1 μg pcDNA3.0-Flag-p53 plasmid to SH-SY5Y cells in the further study. (F) Immunohistochemistry staining showed a significant increment of LC3 (green) under MPP+ stimulation could suppressed by miR-212-5p transfection, which was blocked by p53 overexpression. Scar bar: 40 μm. (G,H) Apoptotic cells were stained by Hoechst 33342 and analysis of positive cells. MiR-212-5p decreased the apoptotic cells by MPP+ stimulation, which was blocked by p53 overexpression. Scale bar: 80 μm. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.01 versus Mock or Mock with NC control group; ##p < 0.01 versus pcDNA3.0-Flag-p53 plasmid plus MPP+ group.CC BY · PubMed Central
FIGURE 6 MiR-212-5p decreases SIRT2 expression and attenuates DA neuron loss in vivo. (A) Fluorescent image of Cy3-labeled miR-212-5p (red) and TH-marked neurons (green) was observed in the SNc of mice. (B) RT-PCR analysis of miR-212-5p. (C,E) Representative microphotographs and quantitative analysis of TH in the SNc of MPTP injured mice. Scar bar: 200 μm. (D,F) Western blotting and quantitative analysis showed that DAT was decreased by MPTP-induced PD mice model, which was reversed by miR-212-5p treatment. (G,H) Western blotting and quantitative analysis of SIRT2 and SIRT1. Consistent with the previous founds, SIRT2 was increased and SIRT1 was decreased in MPTP-induce PD mice model. MiR-212-5p treatment decreased SIRT2 expression with no influence on SIRT1. Data are presented as the mean ± SEM for each group of five mice, Two-way ANOVA, ∗p < 0.05, ∗∗p < 0.01 versus NC with saline treatment; #p < 0.05, ##p < 0.01, ###p < 0.001 versus NC with MPTP-treatment.
FIGURE 6 MiR-212-5p decreases SIRT2 expression and attenuates DA neuron loss in vivo. (A) Fluorescent image of Cy3-labeled miR-212-5p (red) and TH-marked neurons (green) was observed in the SNc of mice. (B) RT-PCR analysis of miR-212-5p. (C,E) Representative microphotographs and quantitative analysis of TH in the SNc of MPTP injured mice. Scar bar: 200 μm. (D,F) Western blotting and quantitative analysis showed that DAT was decreased by MPTP-induced PD mice model, which was reversed by miR-212-5p treatment. (G,H) Western blotting and quantitative analysis of SIRT2 and SIRT1. Consistent with the previous founds, SIRT2 was increased and SIRT1 was decreased in MPTP-induce PD mice model. MiR-212-5p treatment decreased SIRT2 expression with no influence on SIRT1. Data are presented as the mean ± SEM for each group of five mice, Two-way ANOVA, ∗p < 0.05, ∗∗p < 0.01 versus NC with saline treatment; #p < 0.05, ##p < 0.01, ###p < 0.001 versus NC with MPTP-treatment.CC BY · PubMed Central
FIGURE 7 MiR-212-5p promotes p53-dependent autophagy and inhibits apoptosis in vivo. (A) Transmission electron microscope of midbrain in mice. Yellow arrow means autolysosome, red arrow means mitochondrion. (B–D) Representative immunoblots and quantification of midbrain extracts for analysis of LC3B and P62 in mice of both normal and MPTP-treatment. (E) TUNEL staining of midbrain in mice. (F–H) Representative immunoblots and quantification of midbrain extracts for analysis of cleaved caspase-3, Bcl-2 and BAX. (I–K) Western blotting and quantitative analysis showed that miR-212-5p decreased total p53 and increased ace-p53 expression in the midbrain of mice. (L–N) Western blotting and quantitative analysis revealed that miR-212-5p decreased both cytosolic and nuclear p53 expression. Data are presented as the mean ± SEM for each group of five mice. ∗p < 0.05, ∗∗p < 0.01 versus NC with saline treatment; #p < 0.05, ##p < 0.01 versus NC with MPTP-treatment.
FIGURE 7 MiR-212-5p promotes p53-dependent autophagy and inhibits apoptosis in vivo. (A) Transmission electron microscope of midbrain in mice. Yellow arrow means autolysosome, red arrow means mitochondrion. (B–D) Representative immunoblots and quantification of midbrain extracts for analysis of LC3B and P62 in mice of both normal and MPTP-treatment. (E) TUNEL staining of midbrain in mice. (F–H) Representative immunoblots and quantification of midbrain extracts for analysis of cleaved caspase-3, Bcl-2 and BAX. (I–K) Western blotting and quantitative analysis showed that miR-212-5p decreased total p53 and increased ace-p53 expression in the midbrain of mice. (L–N) Western blotting and quantitative analysis revealed that miR-212-5p decreased both cytosolic and nuclear p53 expression. Data are presented as the mean ± SEM for each group of five mice. ∗p < 0.05, ∗∗p < 0.01 versus NC with saline treatment; #p < 0.05, ##p < 0.01 versus NC with MPTP-treatment.CC BY · PubMed Central
FIGURE 8 Schematic illustration demonstrates that miR-212-5p prevents dopaminergic neuron death in the pathogenesis of PD by inhibiting SIRT2. As we find, miR-212-5p is downregulated and specifically regulate the translation of SIRT2 in the midbrain or SH-SY5Y cells of PD experimental models. Furthermore, inhibition of SIRT2 promotes autophagy by decreases cytoplasmic p53 expression. According to p53 is a key deacetylation substrate of SIRT2 and plays a vital role in programmed cell death, regulation of p53 dual function by post-transcriptional regulation of SIRT2 is a potential therapy in PD.
FIGURE 8 Schematic illustration demonstrates that miR-212-5p prevents dopaminergic neuron death in the pathogenesis of PD by inhibiting SIRT2. As we find, miR-212-5p is downregulated and specifically regulate the translation of SIRT2 in the midbrain or SH-SY5Y cells of PD experimental models. Furthermore, inhibition of SIRT2 promotes autophagy by decreases cytoplasmic p53 expression. According to p53 is a key deacetylation substrate of SIRT2 and plays a vital role in programmed cell death, regulation of p53 dual function by post-transcriptional regulation of SIRT2 is a potential therapy in PD.CC BY · PubMed Central

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Metadata

Authors
Sun, S., Han, X., Li, X., Song, Q., Lu, M., Jia, M., Ding, J., & Hu, G.
Venue
Frontiers in Molecular Neuroscience
Publisher
Frontiers Media SA
Published
2018-10-11
Volume
11
ISSN
1662-5099
DOI
10.3389/fnmol.2018.00381
PMC
PMC6193094
Cited by
77
References
6
Licence
creativecommons.org/licenses/by/4.0/ (unspecified)
Funders
National Natural Science Foundation of China (No. 81603091)

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