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Extracellular vesicles derived from astrocyte-treated with haFGF14-154 attenuate Alzheimer phenotype in AD mice

Peng, Dong, Wang, Youjin, Xiao, Yuanjie, Peng, Mengyuan, Mai, Wanwen, Hu, Bo, Jia, Yanbin, Chen, Hongxia, Yang, Yan, Xiang, Qi, Su, Zhijian, Zhang, Qihao, Huang, Yadong·2022·Theranostics
DOI 10.7150/thno.70951PMC PMC9131260
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Figures

Figure 1 AEVs-Aβ+H promote neurite outgrowth and diminish Aβ loading in neurons in vitro. (A) The representative images of MAP2+ cells (red) in rat primary cortical neurons treated with AEVs under the condition of Aβ-injury. (Scale bars, 50 µm). Quantification of the average neurite length of neurons (B), the proportion of the longest length of neural neurites over 100 µm (C) and the number of neural neurites per neuron (D), n = 6. (E) The representative immunoblots of PSD95, GAP43, SYN and Aβ. The quantified expression of PSD95 (F), GAP43 (G), SYN (H) and Aβ (I), n = 6. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test.
Figure 1 AEVs-Aβ+H promote neurite outgrowth and diminish Aβ loading in neurons in vitro. (A) The representative images of MAP2+ cells (red) in rat primary cortical neurons treated with AEVs under the condition of Aβ-injury. (Scale bars, 50 µm). Quantification of the average neurite length of neurons (B), the proportion of the longest length of neural neurites over 100 µm (C) and the number of neural neurites per neuron (D), n = 6. (E) The representative immunoblots of PSD95, GAP43, SYN and Aβ. The quantified expression of PSD95 (F), GAP43 (G), SYN (H) and Aβ (I), n = 6. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test.CC BY · PubMed Central
Figure 2 AEVs-Aβ+H ameliorate cognitive behavior deficits and promote synaptic plasticity in APP/PS1 mice. (A) Schedule of intranasal administration and behavior test of APP/PS1 mice. (B) Spontaneous alternation in Y-maze (n = 6-8). (C) The representative movement tracks of escape latency on day 5 in navigation test of MWM. (D-E) The escape latency (n = 8/9). Representative movement tracks in spatial probe test (F), numbers of crossing the removed platform area (G) and time spend in target quadrant (I) in spatial probe test of MWM, n = 8/9. (H) The representative images of synaptic structure in CA1 region of hippocampus observed by TEM. The length (J) and width (K) of PSD were quantified from 7 random fields per slide, 1 slide per animal, and 3 animals per group (n = 21). Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test and two-way ANOVA with Tukey's post-hoc test.
Figure 2 AEVs-Aβ+H ameliorate cognitive behavior deficits and promote synaptic plasticity in APP/PS1 mice. (A) Schedule of intranasal administration and behavior test of APP/PS1 mice. (B) Spontaneous alternation in Y-maze (n = 6-8). (C) The representative movement tracks of escape latency on day 5 in navigation test of MWM. (D-E) The escape latency (n = 8/9). Representative movement tracks in spatial probe test (F), numbers of crossing the removed platform area (G) and time spend in target quadrant (I) in spatial probe test of MWM, n = 8/9. (H) The representative images of synaptic structure in CA1 region of hippocampus observed by TEM. The length (J) and width (K) of PSD were quantified from 7 random fields per slide, 1 slide per animal, and 3 animals per group (n = 21). Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test and two-way ANOVA with Tukey's post-hoc test.CC BY · PubMed Central
Figure 3 AEVs-Aβ+H enhance the expression of synaptic proteins and alleviate brain Aβ burden in APP/PS1 mice. (A-H) The expression of PSD95, GAP43 and SYN in the prefrontal cortex (PFC) (A) and hippocampus (E) of APP/PS1 mice with intranasal administration of AEVs. The relative expression quantification of PSD95 (B), GAP43 (C), SYN (D) in the PFC and PSD95 (F), GAP43 (G), SYN (H) in hippocampus, n = 8-10. (I) The representative images of Aβ plaque in the dentate gyrus (DG), CA1 and CA3 regions of hippocampus (Scale: 100 µm). (J-L) The area of Aβ plaque is analyzed by image-pro plus software, n = 5-7. (M) Aβ in the PFC and hippocampus were detected by western blot. The quantified expression of Aβ in the PFC (N) and hippocampus (O), n = 8-10. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test.
Figure 3 AEVs-Aβ+H enhance the expression of synaptic proteins and alleviate brain Aβ burden in APP/PS1 mice. (A-H) The expression of PSD95, GAP43 and SYN in the prefrontal cortex (PFC) (A) and hippocampus (E) of APP/PS1 mice with intranasal administration of AEVs. The relative expression quantification of PSD95 (B), GAP43 (C), SYN (D) in the PFC and PSD95 (F), GAP43 (G), SYN (H) in hippocampus, n = 8-10. (I) The representative images of Aβ plaque in the dentate gyrus (DG), CA1 and CA3 regions of hippocampus (Scale: 100 µm). (J-L) The area of Aβ plaque is analyzed by image-pro plus software, n = 5-7. (M) Aβ in the PFC and hippocampus were detected by western blot. The quantified expression of Aβ in the PFC (N) and hippocampus (O), n = 8-10. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test.CC BY · PubMed Central
Figure 4 aFGF down-regulates the level of miR-206-3p targeting BDNF in AEVs secreted in AD microenvironment. (A) Heatmap of miRNA expression profile showing the expression difference in AEVs-Ctrl, AEVs-Aβ and AEVs-Aβ+H by color bar. Red represents increased expression and blue represents decreased expression. Scale is 1.0 to -1.0. (B) Heatmap image displays the significant difference of miRNAs in AEVs-Ctrl, AEVs-Aβ and AEVs-Aβ+H, and the miRNA level is showed as number in each square. (C) Representative signaling pathways of genes targeted by significantly differential miRNAs according to KEGG analysis. (D) The differential miRNAs verified by qPCR in AEVs, n = 3-5. (E) The expression of miR-206-3p detected by qPCR in astrocytes damaged by Aβ accompanied with haFGF14-154 treatment, n = 3. (F) Comparison of miR-206-3p level between neurons and astrocytes subjected to Aβ1-42 oligomer, n = 3/4. (G) The distribution of miR-206-3p (green) in the PFC and hippocampal DG region of APP/PS1 mice measured by FISH and the quantified levels in the PFC (H) and DG region (I), n = 4/5. (J) The plasma miR-206-3p level detected by qPCR in wild-type mice and APP/PS1 mice with intranasal administration of AEVs or PBS, n = 6-8. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test and two-way ANOVA with Tukey's post-hoc test.
Figure 4 aFGF down-regulates the level of miR-206-3p targeting BDNF in AEVs secreted in AD microenvironment. (A) Heatmap of miRNA expression profile showing the expression difference in AEVs-Ctrl, AEVs-Aβ and AEVs-Aβ+H by color bar. Red represents increased expression and blue represents decreased expression. Scale is 1.0 to -1.0. (B) Heatmap image displays the significant difference of miRNAs in AEVs-Ctrl, AEVs-Aβ and AEVs-Aβ+H, and the miRNA level is showed as number in each square. (C) Representative signaling pathways of genes targeted by significantly differential miRNAs according to KEGG analysis. (D) The differential miRNAs verified by qPCR in AEVs, n = 3-5. (E) The expression of miR-206-3p detected by qPCR in astrocytes damaged by Aβ accompanied with haFGF14-154 treatment, n = 3. (F) Comparison of miR-206-3p level between neurons and astrocytes subjected to Aβ1-42 oligomer, n = 3/4. (G) The distribution of miR-206-3p (green) in the PFC and hippocampal DG region of APP/PS1 mice measured by FISH and the quantified levels in the PFC (H) and DG region (I), n = 4/5. (J) The plasma miR-206-3p level detected by qPCR in wild-type mice and APP/PS1 mice with intranasal administration of AEVs or PBS, n = 6-8. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test and two-way ANOVA with Tukey's post-hoc test.CC BY · PubMed Central
Figure 5 miR-206-3p inhibitors promote neurite growth. (A) Representative morphology of MAP2+ cells in primary cortical neurons (red) transfected with miR-206-3p mimics and inhibitors (Scale bars: 50 µm). Quantification of the average neurite length of neurons (B), the proportion of the longest length of neural neurites over 100 µm (C) and the number of neural neurites per neuron (D), n = 6. (E-H) The expression of PSD95, GAP43 and SYN in rat primary cortical neurons transfected with miR-206-3p mimics and inhibitors, n = 6. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by student's t-test.
Figure 5 miR-206-3p inhibitors promote neurite growth. (A) Representative morphology of MAP2+ cells in primary cortical neurons (red) transfected with miR-206-3p mimics and inhibitors (Scale bars: 50 µm). Quantification of the average neurite length of neurons (B), the proportion of the longest length of neural neurites over 100 µm (C) and the number of neural neurites per neuron (D), n = 6. (E-H) The expression of PSD95, GAP43 and SYN in rat primary cortical neurons transfected with miR-206-3p mimics and inhibitors, n = 6. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by student's t-test.CC BY · PubMed Central
Figure 6 miR-206-3p antagomirs alleviate learning and memory deficits in AD mice. (A) Schematic protocol for the hippocampal injection of miR-206-3p antagomirs and behavior test. (B-C) miR-206-3p level in the PFC (B, n = 4) and hippocampus (C, n = 6) of AD mice with brain injection of miR-206-3p antagomirs. (D) The representative movement tracks of escape latency on day 5 in navigation test of MWM. (F) The escape latencies of mice. Representative movement tracks in spatial probe test (E), numbers of crossing the removed platform area (G) and time spend in target quadrant (H) in spatial probe test of MWM, n = 9/10. (I) Spontaneous alternation in Y-maze, n = 9-12. The expression of PSD95, GAP43 and SYN in the PFC (J-M) and hippocampus (N-Q) of AD mice with brain injection of miR-206-3p antagomirs and antagomir NC, n = 8/9. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test and two-way ANOVA with Tukey's post-hoc test.
Figure 6 miR-206-3p antagomirs alleviate learning and memory deficits in AD mice. (A) Schematic protocol for the hippocampal injection of miR-206-3p antagomirs and behavior test. (B-C) miR-206-3p level in the PFC (B, n = 4) and hippocampus (C, n = 6) of AD mice with brain injection of miR-206-3p antagomirs. (D) The representative movement tracks of escape latency on day 5 in navigation test of MWM. (F) The escape latencies of mice. Representative movement tracks in spatial probe test (E), numbers of crossing the removed platform area (G) and time spend in target quadrant (H) in spatial probe test of MWM, n = 9/10. (I) Spontaneous alternation in Y-maze, n = 9-12. The expression of PSD95, GAP43 and SYN in the PFC (J-M) and hippocampus (N-Q) of AD mice with brain injection of miR-206-3p antagomirs and antagomir NC, n = 8/9. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test and two-way ANOVA with Tukey's post-hoc test.CC BY · PubMed Central
Figure 7 miR-206-3p antagomirs reduce the deposition of Aβ in AD mice. (A) Representative images of Aβ plaque in the DG, CA1 and CA3 regions of AD mice with hippocampal injection of miR-206-3p antagomirs (Scale: 100 µm). (B-D) Quantitative analysis for Aβ plaque area by image-pro plus software, n = 3-5. (E-G) The level of Aβ in the PFC and hippocampal tissue of AD mice, n = 5-6. Data are as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test.
Figure 7 miR-206-3p antagomirs reduce the deposition of Aβ in AD mice. (A) Representative images of Aβ plaque in the DG, CA1 and CA3 regions of AD mice with hippocampal injection of miR-206-3p antagomirs (Scale: 100 µm). (B-D) Quantitative analysis for Aβ plaque area by image-pro plus software, n = 3-5. (E-G) The level of Aβ in the PFC and hippocampal tissue of AD mice, n = 5-6. Data are as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test.CC BY · PubMed Central
Figure 8 AEVs-Aβ+H and miR-206-3p antagomirs increase BDNF levels. (A) Potential binding sites in 3'UTR of BDNF. (B) Identification of miR-206-3p potential binding sites to BDNF 3'UTR performed by luciferase reporter assay, n = 4. (C-D) The expression of BDNF in rat primary cortical neurons transfected with miR-206-3p mimics and inhibitors, n = 4. (E-G) BDNF expression in the PFC and hippocampus of APP/PS1 with intranasal administration of AEVs, n = 8-10. (H-J) The expression of BDNF in the PFC and hippocampus of AD mice with hippocampal injection of miR-206-3p antagomirs and antagomir NC, n = 8/9. (K-M) The level of AEP (full-length and cleaved AEP) in the PFC and hippocampus of APP/PS1 mice with intranasal administration of AEVs, n = 8-10. (N-P) The level of AEP (full-length and cleaved AEP) in the PFC and hippocampus of AD mice with hippocampal injection of miR-206-3p antagomirs, n = 11/12. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test.
Figure 8 AEVs-Aβ+H and miR-206-3p antagomirs increase BDNF levels. (A) Potential binding sites in 3'UTR of BDNF. (B) Identification of miR-206-3p potential binding sites to BDNF 3'UTR performed by luciferase reporter assay, n = 4. (C-D) The expression of BDNF in rat primary cortical neurons transfected with miR-206-3p mimics and inhibitors, n = 4. (E-G) BDNF expression in the PFC and hippocampus of APP/PS1 with intranasal administration of AEVs, n = 8-10. (H-J) The expression of BDNF in the PFC and hippocampus of AD mice with hippocampal injection of miR-206-3p antagomirs and antagomir NC, n = 8/9. (K-M) The level of AEP (full-length and cleaved AEP) in the PFC and hippocampus of APP/PS1 mice with intranasal administration of AEVs, n = 8-10. (N-P) The level of AEP (full-length and cleaved AEP) in the PFC and hippocampus of AD mice with hippocampal injection of miR-206-3p antagomirs, n = 11/12. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test.CC BY · PubMed Central
Figure 9 haFGF14-154 inhibits AEP activity via miR-206-3p/BDNF pathway in the brain of APP/PS1 mice. (A-C) miR-206-3p level in the PFC and hippocampal DG region of APP/PS1 mice with intranasal administration of 600 µg/kg haFGF14-154-loaded cationic liposomes (L+H600) or 0.9% saline (vehicle), measured by fluorescence in situ hybridization (FISH), n = 4/5. (D-F) The expression of BDNF and AEP (full-length and cleaved AEP) in the PFC of APP/PS1 mice with intranasal administration of L+H600 or vehicle, n = 6. The plasma levels of miR-206-3p (G) and BDNF (H) in patients with Alzheimer's disease (AD), PD and Schizophrienia detected by qPCR. P values are calculated by age-adjusted ANCOVA model with Tukey's post-hoc test. n = 25/16, 18/18, 15/13 and 12/8 for normal control and patients with AD, PD and Schizophrienia in the experiments of qPCR and ELISA, respectively. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test and student's t-test.
Figure 9 haFGF14-154 inhibits AEP activity via miR-206-3p/BDNF pathway in the brain of APP/PS1 mice. (A-C) miR-206-3p level in the PFC and hippocampal DG region of APP/PS1 mice with intranasal administration of 600 µg/kg haFGF14-154-loaded cationic liposomes (L+H600) or 0.9% saline (vehicle), measured by fluorescence in situ hybridization (FISH), n = 4/5. (D-F) The expression of BDNF and AEP (full-length and cleaved AEP) in the PFC of APP/PS1 mice with intranasal administration of L+H600 or vehicle, n = 6. The plasma levels of miR-206-3p (G) and BDNF (H) in patients with Alzheimer's disease (AD), PD and Schizophrienia detected by qPCR. P values are calculated by age-adjusted ANCOVA model with Tukey's post-hoc test. n = 25/16, 18/18, 15/13 and 12/8 for normal control and patients with AD, PD and Schizophrienia in the experiments of qPCR and ELISA, respectively. Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. P values are calculated by one-way ANOVA with Tukey's post-hoc test and student's t-test.CC BY · PubMed Central

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Metadata

Authors
Peng, D., Wang, Y., Xiao, Y., Peng, M., Mai, W., Hu, B., Jia, Y., Chen, H., Yang, Y., Xiang, Q., Su, Z., Zhang, Q., & Huang, Y.
Venue
Theranostics
Publisher
Ivyspring International Publisher
Published
2022
Volume
12
Issue
8
Pages
3862-3881
ISSN
1838-7640
DOI
10.7150/thno.70951
PMC
PMC9131260
Cited by
52
References
8
Language
en

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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