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Differential spatio-temporal regulation of MMPs in the 5xFAD mouse model of Alzheimer’s disease: evidence for a pro-amyloidogenic role of MT1-MMP

Py, Nathalie A., Bonnet, Amandine E., Bernard, Anne, Marchalant, Yannick, Charrat, Eliane, Checler, Frédéric, Khrestchatisky, Michel, Baranger, Kévin, Rivera, Santiago·2014·Frontiers in Aging Neuroscience
DOI 10.3389/fnagi.2014.00247PMC PMC4166961
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Figure 1 mRNA expression of different proteolytic systems and inflammatory markers across age in 5xFAD mice hippocampi. mRNA expression for MMPs (A) ADAMs (B) Aβ-degrading enzymes (C), TIMPs (D) and inflammatory markers (E) was analyzed in the hippocampus of WT and 5xFAD mice at 2, 4 and 6 months. Values are the mean ± SEM of four mice per group representing fold change differences between genotypes. *p < 0.05, **p < 0.01, ***p < 0.001 when comparing 5xFAD vs. WT of the same age; #p < 0.05, ##p < 0.01, ###p < 0.001 when comparing different ages of the same genotype; ANOVA followed by Tukey’s test.
Figure 1 mRNA expression of different proteolytic systems and inflammatory markers across age in 5xFAD mice hippocampi. mRNA expression for MMPs (A) ADAMs (B) Aβ-degrading enzymes (C), TIMPs (D) and inflammatory markers (E) was analyzed in the hippocampus of WT and 5xFAD mice at 2, 4 and 6 months. Values are the mean ± SEM of four mice per group representing fold change differences between genotypes. *p < 0.05, **p < 0.01, ***p < 0.001 when comparing 5xFAD vs. WT of the same age; #p < 0.05, ##p < 0.01, ###p < 0.001 when comparing different ages of the same genotype; ANOVA followed by Tukey’s test.CC BY · PubMed Central
Figure 2 Age-dependent changes in MMPs and TIMPs across age in 5xFAD mice hippocampi. Western blots and the corresponding quantifications of MMP-2, MMP-9, TIMP-1 and TIMP-2 in the soluble fraction (A), and of MT1-MMP pro- and active forms in the membrane-enriched fraction (B) of WT and 5xFAD mice hippocampi at 2, 4 and 6 months of age. GAPDH normalized values are the mean ± SEM of four mice per group representing the percentage of variation in optical density (O.D.). *p < 0.05, **p < 0.01, ***p < 0.001 when comparing 5xFAD vs. WT of the same age; #p < 0.05, ##p < 0.01, ###p < 0.001 when comparing the same genotype across age; ANOVA followed by Tukey’s test.
Figure 2 Age-dependent changes in MMPs and TIMPs across age in 5xFAD mice hippocampi. Western blots and the corresponding quantifications of MMP-2, MMP-9, TIMP-1 and TIMP-2 in the soluble fraction (A), and of MT1-MMP pro- and active forms in the membrane-enriched fraction (B) of WT and 5xFAD mice hippocampi at 2, 4 and 6 months of age. GAPDH normalized values are the mean ± SEM of four mice per group representing the percentage of variation in optical density (O.D.). *p < 0.05, **p < 0.01, ***p < 0.001 when comparing 5xFAD vs. WT of the same age; #p < 0.05, ##p < 0.01, ###p < 0.001 when comparing the same genotype across age; ANOVA followed by Tukey’s test.CC BY · PubMed Central
Figure 3 Age-dependent upregulation of MMP-2 expression in astrocytes and amyloid plaques in 5xFAD mice hippocampi. (A) Confocal microphotographs representative of four animals per group showing combined immunohistochemistry with the Aβ specific 6E10 antibody (red) and a MMP-2 specific antibody (green) in the subiculum of WT and 5xFAD mice at 2, 4 and 6 months of age. Note that MMP-2 is upregulated in neural cells with astrocyte morphology in the vicinity of amyloid plaques (arrowhead) as early as 2 months. MMP-2 immunostaining increases with age in 5xFAD mice, and at 4 and 6 months there is partial colocalization with amyloid plaques, as revealed by yellow color (arrows). (B) High power magnifications of 5xFAD subiculum at 2 and 6 months showing non-association and association of MMP-2 with amyloid deposits, respectively. Hoechst (blue) labels cell nuclei. (C) Confocal microphotographs showing localization of MMP-2 (green) to GFAP+ astrocytes (red) of 5xFAD mice. Scale bars: 10 μm.
Figure 3 Age-dependent upregulation of MMP-2 expression in astrocytes and amyloid plaques in 5xFAD mice hippocampi. (A) Confocal microphotographs representative of four animals per group showing combined immunohistochemistry with the Aβ specific 6E10 antibody (red) and a MMP-2 specific antibody (green) in the subiculum of WT and 5xFAD mice at 2, 4 and 6 months of age. Note that MMP-2 is upregulated in neural cells with astrocyte morphology in the vicinity of amyloid plaques (arrowhead) as early as 2 months. MMP-2 immunostaining increases with age in 5xFAD mice, and at 4 and 6 months there is partial colocalization with amyloid plaques, as revealed by yellow color (arrows). (B) High power magnifications of 5xFAD subiculum at 2 and 6 months showing non-association and association of MMP-2 with amyloid deposits, respectively. Hoechst (blue) labels cell nuclei. (C) Confocal microphotographs showing localization of MMP-2 (green) to GFAP+ astrocytes (red) of 5xFAD mice. Scale bars: 10 μm.CC BY · PubMed Central
Figure 4 Age-dependent upregulation of MMP-9 expression in astrocytes and amyloid plaques in 5xFAD mice hippocampi. (A) Confocal microphotographs representative of four animals per group showing combined immunohistochemistry with the Aβ specific 6E10 antibody (red) and a MMP-9 specific antibody (green) in the subiculum of WT and 5xFAD mice at 2, 4 and 6 months of age. Note that at 2 months MMP-9 presents a somato-dendritic distribution in 5xFAD neurons, in contrast with WT where it is essentially somatic. Also, at 2 months MMP-9 shows incipient localization to amyloid plaques, as revealed by yellow color (arrows). MMP-9 immunostaining increases with age in astrocytes of 5xFAD mice, and at 4 and 6 months colocalization with amyloid plaques is noticeable. Hoechst (blue) labels cell nuclei. (B) High power magnifications of 5xFAD subiculum at 2 and 6 months showing age-dependent increased association of MMP-9 with amyloid deposits. (C) Confocal microphotographs showing localization of MMP-9 (green) to GFAP+ astrocytes (red) of 5xFAD mice. Scale bars: 10 μm.
Figure 4 Age-dependent upregulation of MMP-9 expression in astrocytes and amyloid plaques in 5xFAD mice hippocampi. (A) Confocal microphotographs representative of four animals per group showing combined immunohistochemistry with the Aβ specific 6E10 antibody (red) and a MMP-9 specific antibody (green) in the subiculum of WT and 5xFAD mice at 2, 4 and 6 months of age. Note that at 2 months MMP-9 presents a somato-dendritic distribution in 5xFAD neurons, in contrast with WT where it is essentially somatic. Also, at 2 months MMP-9 shows incipient localization to amyloid plaques, as revealed by yellow color (arrows). MMP-9 immunostaining increases with age in astrocytes of 5xFAD mice, and at 4 and 6 months colocalization with amyloid plaques is noticeable. Hoechst (blue) labels cell nuclei. (B) High power magnifications of 5xFAD subiculum at 2 and 6 months showing age-dependent increased association of MMP-9 with amyloid deposits. (C) Confocal microphotographs showing localization of MMP-9 (green) to GFAP+ astrocytes (red) of 5xFAD mice. Scale bars: 10 μm.CC BY · PubMed Central
Figure 5 Age-dependent upregulation of MT1-MMP expression in neurons and amyloid plaques in 5xFAD mice hippocampi. (A) Confocal microphotographs representative of four animals per group showing combined immunohistochemistry with the Aβ specific 6E10 antibody (red) and a MT1-MMP specific antibody (green) in the subiculum of WT and 5xFAD mice at 2, 4 and 6 months of age. MT1-MMP presents a punctate distribution in the neuronal cell layer. MT1-MMP immunostaining increases at 6 months in 5xFAD hippocampi and colocalizes with amyloid plaques at all ages studied, as revealed by yellow color (arrows). Hoechst (blue) labels cell nuclei. (B) High power magnifications of 5xFAD subiculum showing localization of MT1-MMP (green) to MAP-2+ neuronal cell bodies (red, upper panels), and no colocalization with GFAP+ astrocytes (red, lower panels). Scale bars: 10 μm.
Figure 5 Age-dependent upregulation of MT1-MMP expression in neurons and amyloid plaques in 5xFAD mice hippocampi. (A) Confocal microphotographs representative of four animals per group showing combined immunohistochemistry with the Aβ specific 6E10 antibody (red) and a MT1-MMP specific antibody (green) in the subiculum of WT and 5xFAD mice at 2, 4 and 6 months of age. MT1-MMP presents a punctate distribution in the neuronal cell layer. MT1-MMP immunostaining increases at 6 months in 5xFAD hippocampi and colocalizes with amyloid plaques at all ages studied, as revealed by yellow color (arrows). Hoechst (blue) labels cell nuclei. (B) High power magnifications of 5xFAD subiculum showing localization of MT1-MMP (green) to MAP-2+ neuronal cell bodies (red, upper panels), and no colocalization with GFAP+ astrocytes (red, lower panels). Scale bars: 10 μm.CC BY · PubMed Central
Figure 6 MMP gelatinolytic activity is present in amyloid plaques. (A) Confocal microphotographs representative of four animals per group showing combined immunohistochemistry using the Aβ specific 6E10 antibody (red) and gelatin-FITC in situ zymography (green) in the hippocampus of 6-month-old 5xFAD mouse. Note that zones of perfect colocalization (arrows, yellow color) coexist with zones of poor or non-colocalization (arrowheads), often associated with dense core amyloid. (B) Confocal microphotographs showing reduction of gelatinolytic activity (green) in plaques (6E10, red) and granule cells (gc) in the dentate gyrus of 5xFAD mice at 6 months. Lower panels without Hoechst staining show that gelatinolysis is reduced in the amyloid plaque and in granule cells. The graph shows a ~50% reduction in gelatin-FITC signal after GM6001 incubation. Values are the mean ± SEM of four mice per group. *p < 0.05; Student t-test.
Figure 6 MMP gelatinolytic activity is present in amyloid plaques. (A) Confocal microphotographs representative of four animals per group showing combined immunohistochemistry using the Aβ specific 6E10 antibody (red) and gelatin-FITC in situ zymography (green) in the hippocampus of 6-month-old 5xFAD mouse. Note that zones of perfect colocalization (arrows, yellow color) coexist with zones of poor or non-colocalization (arrowheads), often associated with dense core amyloid. (B) Confocal microphotographs showing reduction of gelatinolytic activity (green) in plaques (6E10, red) and granule cells (gc) in the dentate gyrus of 5xFAD mice at 6 months. Lower panels without Hoechst staining show that gelatinolysis is reduced in the amyloid plaque and in granule cells. The graph shows a ~50% reduction in gelatin-FITC signal after GM6001 incubation. Values are the mean ± SEM of four mice per group. *p < 0.05; Student t-test.CC BY · PubMed Central
Figure 7 Age-dependent upregulation of APP, APP CTFs and Aβ trimers in 5xFAD hippocampi. (A) Western blot showing full-length APP levels and the corresponding quantification, using the 22C11 antibody on the soluble fraction of WT and 5xFAD hippocampi at 2, 4 and 6 months. (B) Western blot and the corresponding quantifications of full-length APP, APP CTFs (C99 and C83) and Aβ trimers using the CTF and 6E10 antibodies on membrane-enriched fractions of the same animals. Actin normalized values are the mean ± SEM of four mice per group representing the percentage of variation in optical density (O.D.). *p < 0.05, **p < 0.01, when comparing 5xFAD vs. WT of the same age; #p < 0.05, ##p < 0.01, when comparing the same genotype across age; ANOVA followed by Tukey’s test.
Figure 7 Age-dependent upregulation of APP, APP CTFs and Aβ trimers in 5xFAD hippocampi. (A) Western blot showing full-length APP levels and the corresponding quantification, using the 22C11 antibody on the soluble fraction of WT and 5xFAD hippocampi at 2, 4 and 6 months. (B) Western blot and the corresponding quantifications of full-length APP, APP CTFs (C99 and C83) and Aβ trimers using the CTF and 6E10 antibodies on membrane-enriched fractions of the same animals. Actin normalized values are the mean ± SEM of four mice per group representing the percentage of variation in optical density (O.D.). *p < 0.05, **p < 0.01, when comparing 5xFAD vs. WT of the same age; #p < 0.05, ##p < 0.01, when comparing the same genotype across age; ANOVA followed by Tukey’s test.CC BY · PubMed Central
Figure 8 MT1-MMP and MMP-2 have opposite roles in the regulation of C99 and Aβ in HEKswe cells. (A) Left panel, western blot using a GFP specific antibody illustrates a representative experiment showing equivalent levels of overexpression for MT1-MMP/GFP (MT1) and MMP-2/GFP fusion proteins 48 h post-transfection. Right panel, western blot with the corresponding quantification of APP C99 levels, using the CTF antibody on whole cell lysates of HEKswe cells 48 h after transfection of plasmids coding for GPF, MT1-MMP/GFP and MMP-2/GFP fusion proteins. Actin normalized values are the mean ± SEM of four independent cultures representing the percentage of variation in optical density (O.D.). **p < 0.01, MT1 vs. GFP and MMP-2; ANOVA followed by Tukey’s test. (B) ELISA assay showing opposite effects on Aβ40 levels in the supernatant of HEKswe cells 48 h post-transfection. MT1-MMP significantly induced Aβ production, whereas MMP-2 nearly abolished it. Values are the mean ± SEM of four independent cultures. **p < 0.01, MT1 vs. GFP and MMP-2; ##p < 0.01, MMP-2 vs. GFP. ANOVA followed by Tukey’s test.
Figure 8 MT1-MMP and MMP-2 have opposite roles in the regulation of C99 and Aβ in HEKswe cells. (A) Left panel, western blot using a GFP specific antibody illustrates a representative experiment showing equivalent levels of overexpression for MT1-MMP/GFP (MT1) and MMP-2/GFP fusion proteins 48 h post-transfection. Right panel, western blot with the corresponding quantification of APP C99 levels, using the CTF antibody on whole cell lysates of HEKswe cells 48 h after transfection of plasmids coding for GPF, MT1-MMP/GFP and MMP-2/GFP fusion proteins. Actin normalized values are the mean ± SEM of four independent cultures representing the percentage of variation in optical density (O.D.). **p < 0.01, MT1 vs. GFP and MMP-2; ANOVA followed by Tukey’s test. (B) ELISA assay showing opposite effects on Aβ40 levels in the supernatant of HEKswe cells 48 h post-transfection. MT1-MMP significantly induced Aβ production, whereas MMP-2 nearly abolished it. Values are the mean ± SEM of four independent cultures. **p < 0.01, MT1 vs. GFP and MMP-2; ##p < 0.01, MMP-2 vs. GFP. ANOVA followed by Tukey’s test.CC BY · PubMed Central

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Authors
Py, N. A., Bonnet, A. E., Bernard, A., Marchalant, Y., Charrat, E., Checler, F., Khrestchatisky, M., Baranger, K., & Rivera, S.
Venue
Frontiers in Aging Neuroscience
Publisher
Frontiers Media SA
Published
2014-09-18
Volume
6
ISSN
1663-4365
DOI
10.3389/fnagi.2014.00247
PMC
PMC4166961
Cited by
76
References
13

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