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microRNA-128a dysregulation in transgenic Huntington’s disease monkeys

Kocerha, Jannet, Xu, Yan, Prucha, Melinda S, Zhao, Dongming, Chan, Anthony WS·2014·Molecular Brain
DOI 10.1186/1756-6606-7-46PMC PMC4065582
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Figure 1 Genotype and miRNA profiling analysis from HD monkey brains and human miR-128a expression.A) Genomic DNA (gDNA) was isolated from the frontal cortex of 3 GFP control (C1-C3) and 8 HD monkeys (HD1-HD8). The gDNA was amplified using specific primers for mHTT and the PCR product was analyzed by gel electrophoresis. B) The fold change of HTT mRNA levels for the HD monkeys compared to the controls was quantitated by qPCR. C) Cluster diagram for dysregulated miRNAs in HD transgenic cortex. miRNA expression values (Log2 transformed & normalized microarray probe intensities) of the dysregulated microRNAs (P value < 0.05) in the HD and GFP control monkey cortex were median centered. Green squares represent lower than median levels of gene expression; black squares represent median levels of gene expression; red squares represent higher than median levels of gene expression. Legend units: 1.0 = differs from median probe intensity by one log 2 unit (2-fold). D) qPCR validation for the expression of 4 of the 5 miRNAs with significant Ingenuity analysis association to the HD pathway (miR-940 also showed association with the HD pathway, however, no Taqman assays were commercially available). T-test was used to determine significant differences between HD and control monkeys (P Value < 0.05 indicated by *). E) Expression of miR-128a was quantitated from control, pre-symptomatic (HD), and post-symptomatic (HD) human striatum samples. Total RNA was extracted and probed with specific Taqman primers to miR-128 for qPCR. T-tests were used to determine significant differences compared to the control group (P Value < 0.05 indicated by *).
Figure 1 Genotype and miRNA profiling analysis from HD monkey brains and human miR-128a expression.A) Genomic DNA (gDNA) was isolated from the frontal cortex of 3 GFP control (C1-C3) and 8 HD monkeys (HD1-HD8). The gDNA was amplified using specific primers for mHTT and the PCR product was analyzed by gel electrophoresis. B) The fold change of HTT mRNA levels for the HD monkeys compared to the controls was quantitated by qPCR. C) Cluster diagram for dysregulated miRNAs in HD transgenic cortex. miRNA expression values (Log2 transformed & normalized microarray probe intensities) of the dysregulated microRNAs (P value < 0.05) in the HD and GFP control monkey cortex were median centered. Green squares represent lower than median levels of gene expression; black squares represent median levels of gene expression; red squares represent higher than median levels of gene expression. Legend units: 1.0 = differs from median probe intensity by one log 2 unit (2-fold). D) qPCR validation for the expression of 4 of the 5 miRNAs with significant Ingenuity analysis association to the HD pathway (miR-940 also showed association with the HD pathway, however, no Taqman assays were commercially available). T-test was used to determine significant differences between HD and control monkeys (P Value < 0.05 indicated by *). E) Expression of miR-128a was quantitated from control, pre-symptomatic (HD), and post-symptomatic (HD) human striatum samples. Total RNA was extracted and probed with specific Taqman primers to miR-128 for qPCR. T-tests were used to determine significant differences compared to the control group (P Value < 0.05 indicated by *).CC BY · PubMed Central
Figure 2 Expression of mHTT in monkey frontal cortex. A) Brain sections of HD monkey (rHD4, rHD7 and rHD8) and GFP monkey (C1 and C3) were immunostained with mEM48. Low magnification (upper panels, 40×) and high magnification (lower panels, 100×) shows that mHTT forms intranuclear inclusions (arrows) and neuropil aggregates (arrowheads). B) mEM48 immunoblot of frontal cortex showed high-molecular-mass mutant HTT aggregate (arrow) in the stacking gel. γ- tubulin was used as an internal control. C) Quantification of the mHTT aggregate in the stacking gel showed the relative level of mHTT aggregates in the frontal cortex. All HD monkeys have significantly higher level of mHTT aggregate compared to the controls. D) The percentage of mEM48 positive cells with or without intranuclear inclusions was calculated and compared among HD monkey frontal cortex immunostained with mEM48. HD7 has significantly more nuclei with intranuclear inclusions than HD4 and HD8. The data was presented as mean ± SE. *P < 0.05.
Figure 2 Expression of mHTT in monkey frontal cortex. A) Brain sections of HD monkey (rHD4, rHD7 and rHD8) and GFP monkey (C1 and C3) were immunostained with mEM48. Low magnification (upper panels, 40×) and high magnification (lower panels, 100×) shows that mHTT forms intranuclear inclusions (arrows) and neuropil aggregates (arrowheads). B) mEM48 immunoblot of frontal cortex showed high-molecular-mass mutant HTT aggregate (arrow) in the stacking gel. γ- tubulin was used as an internal control. C) Quantification of the mHTT aggregate in the stacking gel showed the relative level of mHTT aggregates in the frontal cortex. All HD monkeys have significantly higher level of mHTT aggregate compared to the controls. D) The percentage of mEM48 positive cells with or without intranuclear inclusions was calculated and compared among HD monkey frontal cortex immunostained with mEM48. HD7 has significantly more nuclei with intranuclear inclusions than HD4 and HD8. The data was presented as mean ± SE. *P < 0.05.CC BY · PubMed Central
Figure 3 Neuropathology in HD monkey frontal cortex. A-F) An increased number of caspase-3 positive cells in frontal cortex of HD monkeys (D-E) was observed when compared with control monkeys (A-B). C) Quantification of caspase-3 positive cells in HD and control monkey frontal cortex showed significant difference between HD monkeys (HD7 and HD8) and control monkey (C1 or C3). However, no difference was observed between HD4 and the controls. The data are presented as mean ± SE. *P < 0.05 compared with C1, and #P < 0.05 compared with C3. G-L) An increased number and intensity of GFAP positive cells was observed in HD monkeys (HD7 and HD8) but not in HD4 (J-L). High magnification (inserts) showed reactive astrocytes in HD7 and HD8 with strong GFAP staining. Quantification of GFAP expression in the HD monkey frontal cortex showed significant increase expression of GFAP in HD7 and HD8 but not in HD4. The data were presented as mean ± SE. *P < 0.05
Figure 3 Neuropathology in HD monkey frontal cortex. A-F) An increased number of caspase-3 positive cells in frontal cortex of HD monkeys (D-E) was observed when compared with control monkeys (A-B). C) Quantification of caspase-3 positive cells in HD and control monkey frontal cortex showed significant difference between HD monkeys (HD7 and HD8) and control monkey (C1 or C3). However, no difference was observed between HD4 and the controls. The data are presented as mean ± SE. *P < 0.05 compared with C1, and #P < 0.05 compared with C3. G-L) An increased number and intensity of GFAP positive cells was observed in HD monkeys (HD7 and HD8) but not in HD4 (J-L). High magnification (inserts) showed reactive astrocytes in HD7 and HD8 with strong GFAP staining. Quantification of GFAP expression in the HD monkey frontal cortex showed significant increase expression of GFAP in HD7 and HD8 but not in HD4. The data were presented as mean ± SE. *P < 0.05CC BY · PubMed Central
Figure 4 In-vitro analysis of HD-associated miR-128a gene targets. The regulation of the 3’-UTR activity by miR-128 for (A) HIP-1, (B) HTT, (C) SP-1, and (D) GRM-5 was evaluated in 293-FT cells. 293-FT cells were co-transfected with 10 nM pre-miR-128a or negative control (NC) as well as luciferase reporter constructs containing the WT or mutant (MUT) 3’- predicted miR-128a binding site for each of the genes. Relative luciferase activity data were normalized as a percentage of plasmid-only control levels (100%) for each 3’-UTR construct. One-way ANOVA followed by Tukey’s post-hoc testing confirmed that miR-128a exposure resulted in significant reduction (p < 0.001) in 3’-UTR activity for each WT construct (as compared to NC); no significant differences between treatments were detected in MUT constructs.
Figure 4 In-vitro analysis of HD-associated miR-128a gene targets. The regulation of the 3’-UTR activity by miR-128 for (A) HIP-1, (B) HTT, (C) SP-1, and (D) GRM-5 was evaluated in 293-FT cells. 293-FT cells were co-transfected with 10 nM pre-miR-128a or negative control (NC) as well as luciferase reporter constructs containing the WT or mutant (MUT) 3’- predicted miR-128a binding site for each of the genes. Relative luciferase activity data were normalized as a percentage of plasmid-only control levels (100%) for each 3’-UTR construct. One-way ANOVA followed by Tukey’s post-hoc testing confirmed that miR-128a exposure resulted in significant reduction (p < 0.001) in 3’-UTR activity for each WT construct (as compared to NC); no significant differences between treatments were detected in MUT constructs.CC BY · PubMed Central

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Authors
Kocerha, J., Xu, Y., Prucha, M. S., Zhao, D., & Chan, A. W.
Venue
Molecular Brain
Publisher
Springer Science and Business Media LLC
Published
2014-06-13
Volume
7
Issue
1
ISSN
1756-6606
DOI
10.1186/1756-6606-7-46
PMC
PMC4065582
Cited by
75
References
3
Language
en

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Kocerha, J., Xu, Y., Prucha, M. S., Zhao, D., & Chan, A. W. (2014). microRNA-128a dysregulation in transgenic Huntington’s disease monkeys. Molecular Brain. https://doi.org/10.1186/1756-6606-7-46