dsred n1  (Addgene inc)

Journal: Frontiers in Oncology

Article Title: PALB2 deficiency may sensitize H3K27M-mutant pediatric HGG cells to BMN673/talazoparib

doi: 10.3389/fonc.2025.1589396

Figure Lengend Snippet: Analysis of NHEJ activity via the EJ5 reporter assay in SF188 and Res259 cells stably expressing the H3 WT or H3K27M mutation. (A) Schematic representation of the EJ5 reporter for NHEJ repair. EJ5-GFP is shown along with two classes of NHEJ repair products that can restore a GFP expression cassette. In the starting construct, the GFP gene is inactive. GFP expression is only activated when I-Sce1-induced DSBs are successfully repaired via NHEJ. (B) H3K27M-mutant SF188 cells and WT SF188 cells containing the reporter cassette were transfected with the I-SceI and DsRed plasmids. Left panel: Immunofluorescence images of GFP-positive cells and DsRed-positive cells (scale bars, 100 µm). Right panel: NHEJ activity in H3K27M-mutant SF188 cells and WT SF188 cells. (C) H3K27M-mutant Res259 cells and WT Res259 cells containing reporter cassettes were transfected with I-SceI and DsRed plasmids. Left panel: Immunofluorescence images of GFP-positive cells and DsRed-positive cells (scale bars, 100 µm). Right panel: NHEJ activity in H3K27M-mutant Res259 cells and WT Res259 cells. NHEJ activity was determined by normalizing the percentage of eGFP-positive cells to the percentage of DsRed-positive cells. The data are shown as the mean ± SD from three independent experiments. Student’s t test was used to calculate p values. ** p < 0.01 versus the corresponding control.

Article Snippet: The indicated EJ5 reporter cell lines were transfected with two plasmids, namely, the I-SceI expression vector pCBASce (Addgene #26477) and the DsRed expression vector (Addgene #54493), 48 h later, the percentage of GFP-positive cells among DsRed-positive cells was evaluated by imaging with a Carl Zeiss LSM 710 confocal fluorescence microscope and quantified via FACS on a BD AccuriTM C6 flow cytometer (BD Biosciences, USA) using BD AccuriTM software.

Techniques: Activity Assay, Reporter Assay, Stable Transfection, Expressing, Mutagenesis, Construct, Transfection, Immunofluorescence, Control

Journal: Neural Regeneration Research

Article Title: Unilateral rNurr1-V5 transgene expression in nigral dopaminergic neurons mitigates bilateral neuropathology and behavioral deficits in parkinsonian rats with α-synucleinopathy

doi: 10.4103/1673-5374.391190

Figure Lengend Snippet: Overview of the mean values, standard deviation, and sample size per each parameter and treatment group at the date of stratification

Article Snippet: The Nurr1 sequence (1796 bp; GenBank, NM_019328; https://www.ncbi.nlm.nih.gov/search/all/?term=NM_019328) was obtained by a NheI-SpeI digestion from the prNurr1-DsRed2-N1 plasmid and subcloned between the SpeI restriction sites of the pTracer TM-EF/V5-His B plasmid (Invitrogen, Carlsbad, CA, USA).

Techniques: Standard Deviation, Transfection

Journal: Neural Regeneration Research

Article Title: Unilateral rNurr1-V5 transgene expression in nigral dopaminergic neurons mitigates bilateral neuropathology and behavioral deficits in parkinsonian rats with α-synucleinopathy

doi: 10.4103/1673-5374.391190

Figure Lengend Snippet: Local unilateral gene transfection leads to bilateral transgene expression in nigral dopaminergic neurons of parkinsonian rats. (A) Representative micrographs of the injured substantia nigra (Injected side) transfected with NTS-polyplex NPs containing the plasmids pTracer-rNurr1-V5 (prNurr1) or pEGFP-N1 (pEGFP). Non-injected side = the contralateral substantia nigra of the same rat. V5 (green) and TH (red) were identified by indirect immunofluorescence on day 30 after NPs treatment. The scale value is equal for all micrographs. (B) Scatter plots of immunofluorescence area density (IFAD) for V5 and TH measured from micrographs of panel A with the software ImageJ. The values are the mean ± SD from three anatomical levels ( n = 3 independent rats per experimental condition). * P < 0.0001, healthy group vs. other groups. One-way analysis of variance followed by Tukey's post hoc test was used. Healthy: Rats without lesion; prNurr1: rats with BSSG lesion and transfected with pTracer-rNurr1-V5; pEGFP: rats with BSSG lesion and transfected with pEGFP-N1; UT: untransfected parkinsonian rats. BSSG: β-Sitosterol β-D-glucoside; NPs: nanoparticles; ns: not significant; NTS: neurotensin; TH: tyrosine hydroxylase; V5: tag allows detection of rNurr1.

Article Snippet: The Nurr1 sequence (1796 bp; GenBank, NM_019328; https://www.ncbi.nlm.nih.gov/search/all/?term=NM_019328) was obtained by a NheI-SpeI digestion from the prNurr1-DsRed2-N1 plasmid and subcloned between the SpeI restriction sites of the pTracer TM-EF/V5-His B plasmid (Invitrogen, Carlsbad, CA, USA).

Techniques: Transfection, Expressing, Injection, Immunofluorescence, Software

Journal: Neural Regeneration Research

Article Title: Unilateral rNurr1-V5 transgene expression in nigral dopaminergic neurons mitigates bilateral neuropathology and behavioral deficits in parkinsonian rats with α-synucleinopathy

doi: 10.4103/1673-5374.391190

Figure Lengend Snippet: Local unilateral pTracer-rNurr1-V5 transfection bilaterally reduces senescence in dopaminergic neurons of parkinsonian rats. (A) Representative micrographs of the substantia nigra (Injected side) transfected with NTS-polyplex NPs containing pEGFP-N1 (pEGFP) or pTracer-rNurr1-V5 (prNurr1). Non-injected side = the contralateral substantia nigra of the same rat. TH immunohistochemistry and the Sen-β-Gal counterstaining were made on day 30 after transfection (60 days after lesion). The oval dotted line delimits the SNpc area that was quantified. (B) Representative Sen-β-Gal staining images of TH + neurons to show the effect of prNurr1. The scale value is equal for all micrographs. (C) Sen-β-Gal area density quantification of micrographs in panel A using ImageJ software. The values are the mean ± SD from three anatomical levels ( n = 3 independent rats per experimental condition). prNurr1 group vs . UT group (Ω P < 0.001) and pEGFP (£ P < 0.01, ¥ P < 0.001). * P < 0.01, healthy group vs . UT and pEGFP groups. One-way analysis of variance followed by Tukey's post hoc test was used. Healthy: Rats without lesion; prNurr1: rats with BSSG lesion and transfected with pTracer-rNurr1-V5; pEGFP: rats with BSSG lesion and transfected with pEGFP-N1; UT: untransfected parkinsonian rats. BSSG: β-Sitosterol β-D-glucoside; NPs: nanoparticles; ns: not significant; NTS: neurotensin; Sen-β-Gal: senescence-β-Galactosidase; SNpc: substantia nigra pars compacta; TH: tyrosine hydroxylase.

Article Snippet: The Nurr1 sequence (1796 bp; GenBank, NM_019328; https://www.ncbi.nlm.nih.gov/search/all/?term=NM_019328) was obtained by a NheI-SpeI digestion from the prNurr1-DsRed2-N1 plasmid and subcloned between the SpeI restriction sites of the pTracer TM-EF/V5-His B plasmid (Invitrogen, Carlsbad, CA, USA).

Techniques: Transfection, Injection, Immunohistochemistry, Staining, Software

Journal: Neural Regeneration Research

Article Title: Unilateral rNurr1-V5 transgene expression in nigral dopaminergic neurons mitigates bilateral neuropathology and behavioral deficits in parkinsonian rats with α-synucleinopathy

doi: 10.4103/1673-5374.391190

Figure Lengend Snippet: Local unilateral pTracer-rNurr1-V5 transfection bilaterally mitigates the cytoskeleton loss in dopaminergic neurons of parkinsonian rats. (A) Representative micrographs of the substantia nigra (Injected side) transfected with NTS-polyplex NPs containing pEGFP-N1 (pEGFP) or pTracer-rNurr1-V5 (prNurr1). Non-injected side = the contralateral substantia nigra of the same rat. Double immunofluorescence against βIII-tubulin (green) and TH (red) was made on day 30 post-transfection. The scale value is equal for all micrographs. (B) Scatter plots of immunofluorescence area density (IFAD) of βIII-tubulin and TH measured from micrographs of panel A using ImageJ software. The values are the mean ± SD from three anatomical levels ( n = 3 independent rats per experimental condition). P < 0.05, healthy group vs . other groups in TH (*) and βIII tubulin (£). One-way analysis of variance followed by Tukey's post hoc test was used. Healthy: rats without lesion; prNurr1: rats with BSSG lesion and transfected with pTracer-rNurr1-V5; pEGFP: rats with BSSG lesion and transfected with pEGFP-N1; UT: untransfected parkinsonian rats. BSSG: β-Sitosterol β-D-glucoside; NPs: nanoparticles; ns: not significant; NTS: neurotensin; TH: tyrosine hydroxylase.

Article Snippet: The Nurr1 sequence (1796 bp; GenBank, NM_019328; https://www.ncbi.nlm.nih.gov/search/all/?term=NM_019328) was obtained by a NheI-SpeI digestion from the prNurr1-DsRed2-N1 plasmid and subcloned between the SpeI restriction sites of the pTracer TM-EF/V5-His B plasmid (Invitrogen, Carlsbad, CA, USA).

Techniques: Transfection, Injection, Immunofluorescence, Software

Journal: Neural Regeneration Research

Article Title: Unilateral rNurr1-V5 transgene expression in nigral dopaminergic neurons mitigates bilateral neuropathology and behavioral deficits in parkinsonian rats with α-synucleinopathy

doi: 10.4103/1673-5374.391190

Figure Lengend Snippet: Local unilateral pTracer-rNurr1-V5 transfection recovers dopaminergic neurons and branching in parkinsonian rats. NTS-polyplex NPs containing pEGFP-N1 (pEGFP) or pTracer-rNurr1-V5 (prNurr1) were injected in the injured substantia nigra (Injected side) on day 30 post-BSSG lesion. Non-injected side = the contralateral substantia nigra of the same rat. (A) Representative micrographs of nigral dopaminergic neurons and branching revealed by TH immunohistochemistry on day 30 post-transfection in different anatomic levels (displayed at the left in every row). The scale value is equal for all micrographs. Scatter plots of TH + cell counting (B) and immunoreactivity area density (C) measured from micrographs of panel A using ImageJ software. The values are the mean ± SD from five anatomical levels ( n = 3 independent rats per experimental condition). * P < 0.05, healthy group vs . other groups. One-way analysis of variance followed by Tukey's post hoc test was used. Healthy: rats without lesion; prNurr1: rats with BSSG lesion and transfected with pTracer-rNurr1-V5; pEGFP: rats with BSSG lesion and transfected with pEGFP-N1; UT: untransfected parkinsonian rats. BSSG: β-sitosterol β-D-glucoside; NPs: nanoparticles; ns: not significant; NTS: neurotensin; TH: tyrosine hydroxylase.

Article Snippet: The Nurr1 sequence (1796 bp; GenBank, NM_019328; https://www.ncbi.nlm.nih.gov/search/all/?term=NM_019328) was obtained by a NheI-SpeI digestion from the prNurr1-DsRed2-N1 plasmid and subcloned between the SpeI restriction sites of the pTracer TM-EF/V5-His B plasmid (Invitrogen, Carlsbad, CA, USA).

Techniques: Transfection, Injection, Immunohistochemistry, Cell Counting, Software

Journal: Neural Regeneration Research

Article Title: Unilateral rNurr1-V5 transgene expression in nigral dopaminergic neurons mitigates bilateral neuropathology and behavioral deficits in parkinsonian rats with α-synucleinopathy

doi: 10.4103/1673-5374.391190

Figure Lengend Snippet: Unilateral pTracer-rNurr1-V5 transfection bilaterally recovers dopaminergic striatal terminals in parkinsonian rats. NTS-polyplex NPs containing pEGFP-N1 (pEGFP) or pTracer-rNurr1-V5 (prNurr1) were injected in the injured substantia nigra (Injected side) on day 30 post-BSSG lesion. Non-injected side = the contralateral substantia nigra of the same rat. (A) Representative micrographs of the striatal dopaminergic ramifications revealed by TH immunohistochemistry on day 30 post-transfection in different anatomic levels (displayed at the left in every row) according to Paxinos and Watson Atlas. The scale value is equal for all micrographs. (B) Scatter plots of TH immunoreactivity area density measured from micrographs of panel A using ImageJ software. The values are the mean ± SD from five anatomical levels ( n = 3 independent rats per experimental condition). * P < 0.01, healthy group vs . other groups. One-way analysis of variance followed by Tukey's post hoc test was used. Healthy: rats without lesion; prNurr1: rats with BSSG lesion and transfected with pTracer-rNurr1-V5; pEGFP: Rats with BSSG lesion and transfected with pEGFP-N1; UT: untransfected parkinsonian rats. BSSG: β-Sitosterol β-D-glucoside; NPs: nanoparticles; ns: not significant; NTS: neurotensin; TH: tyrosine hydroxylase.

Article Snippet: The Nurr1 sequence (1796 bp; GenBank, NM_019328; https://www.ncbi.nlm.nih.gov/search/all/?term=NM_019328) was obtained by a NheI-SpeI digestion from the prNurr1-DsRed2-N1 plasmid and subcloned between the SpeI restriction sites of the pTracer TM-EF/V5-His B plasmid (Invitrogen, Carlsbad, CA, USA).

Techniques: Transfection, Injection, Immunohistochemistry, Software

Journal: Neural Regeneration Research

Article Title: Unilateral rNurr1-V5 transgene expression in nigral dopaminergic neurons mitigates bilateral neuropathology and behavioral deficits in parkinsonian rats with α-synucleinopathy

doi: 10.4103/1673-5374.391190

Figure Lengend Snippet: Unilateral pTracer-rNurr1-V5 transfection bilaterally restores BDNF levels in nigral dopamine neurons of parkinsonian rats. NTS-polyplex NPs containing pEGFP-N1 (pEGFP) or pTracer-rNurr1-V5 (prNurr1) were injected in the injured substantia nigra (injected side) 30 days post-BSSG lesion. Non-injected side = the contralateral substantia nigra of the same rat. (A) Representative micrographs of the SNpc with BDNF (green) and TH (red) double immunofluorescence against BDNF and TH on day 30 post-transfection. The scale value is equal for all micrographs. (B) Immunofluorescence area density (IFAD) for BDNF and TH was determined using ImageJ software. The values are the mean ± SD from three anatomical levels ( n = 3 independent rats per experimental condition). P < 0.01, healthy group vs. other groups in TH (*) and BDNF (£). One-way analysis of variance followed by Tukey's post hoc test was used. Healthy: Rats without lesion; prNurr1: rats with BSSG lesion and transfected with pTracer-rNurr1-V5; pEGFP: rats with BSSG lesion and transfected with pEGFP-N1; UT: untransfected parkinsonian rats. BDNF: Brain-derived neurotrophic factor; BSSG: β-sitosterol β-D-glucoside; NPs: nanoparticles; ns: not significant; NTS: neurotensin; SNpc: substantia nigra pars compacta; TH: tyrosine hydroxylase.

Article Snippet: The Nurr1 sequence (1796 bp; GenBank, NM_019328; https://www.ncbi.nlm.nih.gov/search/all/?term=NM_019328) was obtained by a NheI-SpeI digestion from the prNurr1-DsRed2-N1 plasmid and subcloned between the SpeI restriction sites of the pTracer TM-EF/V5-His B plasmid (Invitrogen, Carlsbad, CA, USA).

Techniques: Transfection, Injection, Immunofluorescence, Software, Derivative Assay

Journal: Neural Regeneration Research

Article Title: Unilateral rNurr1-V5 transgene expression in nigral dopaminergic neurons mitigates bilateral neuropathology and behavioral deficits in parkinsonian rats with α-synucleinopathy

doi: 10.4103/1673-5374.391190

Figure Lengend Snippet: Local unilateral pTracer-rNurr1-V5 transfection decreases the bilateral α-synuclein aggregation in the substantia nigra and striatum. NTS-polyplex NPs containing pEGFP-N1 (pEGFP) or pTracer-rNurr1-V5 (prNurr1) were injected in the injured SN (Injected side) after 30 days post-BSSG lesion. Non-injected side = the contralateral SN of the same rat. (A) Representative micrographs of the SNpc and striatum with α-synuclein aggregates displayed by immunohistochemistry on day 30 post-transfection. The scale value is equal for all micrographs. (B) Scatter plots of α-synuclein aggregation shown through immunoreactivity area density measured from micrographs of panel A using ImageJ software. The values are the mean ± SD from three anatomical levels ( n = 3 independent rats per experimental condition). * P < 0.05, healthy group vs. UT and pEGFP groups. One-way analysis of variance followed by Tukey's post hoc test was used. (C) Immunofluorescence images show a reduction of α-synuclein immunoreactivity (red) and Thioflavin T counterstaining (green) in the SNpc on day 30 after pTracer-rNurr1-V5 transfection. Healthy: rats without lesion; prNurr1: rats with BSSG lesion and transfected with pTracer-rNurr1-V5; pEGFP: rats with BSSG lesion and transfected with pEGFP-N1; UT: untransfected parkinsonian rats. BSSG: β-Sitosterol β-D-glucoside; NPs: nanoparticles; ns: not significant; NTS: neurotensin; SN: substantia nigra; SNpc: substantia nigra pars compacta; α-syn: α-synuclein.

Article Snippet: The Nurr1 sequence (1796 bp; GenBank, NM_019328; https://www.ncbi.nlm.nih.gov/search/all/?term=NM_019328) was obtained by a NheI-SpeI digestion from the prNurr1-DsRed2-N1 plasmid and subcloned between the SpeI restriction sites of the pTracer TM-EF/V5-His B plasmid (Invitrogen, Carlsbad, CA, USA).

Techniques: Transfection, Injection, Immunohistochemistry, Software, Immunofluorescence

Journal: Neural Regeneration Research

Article Title: Unilateral rNurr1-V5 transgene expression in nigral dopaminergic neurons mitigates bilateral neuropathology and behavioral deficits in parkinsonian rats with α-synucleinopathy

doi: 10.4103/1673-5374.391190

Figure Lengend Snippet: Unilateral pTracer-rNurr1-V5 transfection halts bilaterally microglial activation in the substantia nigra. NTS-polyplex NPs containing pEGFP-N1 (pEGFP) or pTracer-rNurr1-V5 (prNurr1) were injected in the injured SN (Injected side) on day 30 post-BSSG lesion. Non-injected side = the contralateral SN of the same rat. (A) Representative micrographs of activated microglia revealed by Iba1 immunoreactivity in the SN on day 30 post-transfection. The scale value is equal for all micrographs. (B) Scatter plots of Iba1 immunoreactivity area density measured from micrographs of panel A using ImageJ software. The values are the mean ± SD from three anatomical levels ( n = 3 independent rats per experimental condition). * P < 0.01, healthy group vs . UT and pEGFP groups. One-way analysis of variance followed by Tukey's post hoc test was used. Healthy: Rats without lesion; prNurr1: rats with BSSG lesion and transfected with pTracer-rNurr1-V5; pEGFP: rats with BSSG lesion and transfected with pEGFP-N1; UT: untransfected parkinsonian rats. BSSG: β-Sitosterol β-D-glucoside; Iba1: ionized calcium-binding adaptor molecule 1; NPs: nanoparticles; ns: not significant; NTS: neurotensin; SN: substantia nigra.

Article Snippet: The Nurr1 sequence (1796 bp; GenBank, NM_019328; https://www.ncbi.nlm.nih.gov/search/all/?term=NM_019328) was obtained by a NheI-SpeI digestion from the prNurr1-DsRed2-N1 plasmid and subcloned between the SpeI restriction sites of the pTracer TM-EF/V5-His B plasmid (Invitrogen, Carlsbad, CA, USA).

Techniques: Transfection, Activation Assay, Injection, Software, Binding Assay

Journal: Neural Regeneration Research

Article Title: Unilateral rNurr1-V5 transgene expression in nigral dopaminergic neurons mitigates bilateral neuropathology and behavioral deficits in parkinsonian rats with α-synucleinopathy

doi: 10.4103/1673-5374.391190

Figure Lengend Snippet: Unilateral pTracer-rNurr1-V5 transfection bilaterally halts neurotoxic A1 astrocyte induction in the substantia nigra of parkinsonian rats. NTS-polyplex NPs containing pEGFP-N1 (pEGFP) or pTracer-rNurr1-V5 (prNurr1) were injected in the injured SN (Injected side) on day 30 post-BSSG lesion. Non-injected side = the contralateral SN of the same rat. (A) Representative micrographs of the substantia nigra with C3-GFAP double immunofluorescence on day 30 post-transfection. The scale bar is equal for all micrographs. (B) Immunofluorescence area density (IFAD) for C3 (green) and GFAP (red) was quantified using ImageJ software. The values are the mean ± SD from three anatomical levels ( n = 3 independent rats per experimental condition). P < 0.0001, healthy group vs . UT and pEGFP groups in GFAP (*) and C3 (£). One-way analysis of variance followed by Tukey's post hoc test was used. (C) Amplified merged images show the reduction of C3 immunoreactivity in GFAP cells with nuclear Hoechst counterstaining (blue) in the SNpc on day 30 after pTracer-rNurr1-V5 transfection. Healthy: Rats without lesion; prNurr1: rats with BSSG lesion and transfected with pTracer-rNurr1-V5; pEGFP: rats with BSSG lesion and transfected with pEGFP-N1; UT: untransfected parkinsonian rats. BSSG: β-Sitosterol β-D-glucoside; C3: complement component 3; GFAP: glial fibrillary acidic protein; NPs: nanoparticles; ns: not significant; NTS: neurotensin; SN: substantia nigra; SNpc: substantia nigra pars compacta.

Article Snippet: The Nurr1 sequence (1796 bp; GenBank, NM_019328; https://www.ncbi.nlm.nih.gov/search/all/?term=NM_019328) was obtained by a NheI-SpeI digestion from the prNurr1-DsRed2-N1 plasmid and subcloned between the SpeI restriction sites of the pTracer TM-EF/V5-His B plasmid (Invitrogen, Carlsbad, CA, USA).

Techniques: Transfection, Injection, Immunofluorescence, Software, Amplification

Journal: Neural Regeneration Research

Article Title: Unilateral rNurr1-V5 transgene expression in nigral dopaminergic neurons mitigates bilateral neuropathology and behavioral deficits in parkinsonian rats with α-synucleinopathy

doi: 10.4103/1673-5374.391190

Figure Lengend Snippet: Unilateral pTracer-rNurr1-V5 transfection bilaterally induces neurotrophic A2 astrocyte in the substantia nigra. NTS-polyplex NPs containing pEGFP-N1 (pEGFP) or pTracer-rNurr1-V5 (prNurr1) were injected in the injured SN (Injected side) on day 30 post-BSSG lesion. Non-injected side = the contralateral SN of the same rat. (A) Representative micrographs of SN with S100A10-GFAP double immunofluorescence on day 30 post-transfection. The scale bar is equal for all micrographs. (B) Immunofluorescence area density (IFAD) for S100A10 (green) and GFAP (red) was measured with ImageJ software. The values are the mean ± SD from three anatomical levels ( n = 3 independent rats per experimental condition). * P < 0.001, healthy group vs . other groups. One-way analysis of variance followed by Tukey's post hoc test was used. (C) Immunofluorescence images show the increase of S100A10 immunoreactivity in GFAP cells with nuclear Hoechst counterstaining (blue) in the SNpc on day 30 after pTracer-rNurr1-V5 transfection. Healthy: Rats without lesion; prNurr1: rats with BSSG lesion and transfected with pTracer-rNurr1-V5; pEGFP: rats with BSSG lesion and transfected with pEGFP-N1; UT: untransfected parkinsonian rats. BSSG: β-Sitosterol β-D-glucoside; GFAP: glial fibrillary acidic protein; NPs: nanoparticles; ns: not significant; NTS: neurotensin; S100A10: S100 calcium-binding protein A10; SN: substantia nigra; SNpc: substantia nigra pars compacta.

Article Snippet: The Nurr1 sequence (1796 bp; GenBank, NM_019328; https://www.ncbi.nlm.nih.gov/search/all/?term=NM_019328) was obtained by a NheI-SpeI digestion from the prNurr1-DsRed2-N1 plasmid and subcloned between the SpeI restriction sites of the pTracer TM-EF/V5-His B plasmid (Invitrogen, Carlsbad, CA, USA).

Techniques: Transfection, Injection, Immunofluorescence, Software, Binding Assay

Journal: Neural Regeneration Research

Article Title: Unilateral rNurr1-V5 transgene expression in nigral dopaminergic neurons mitigates bilateral neuropathology and behavioral deficits in parkinsonian rats with α-synucleinopathy

doi: 10.4103/1673-5374.391190

Figure Lengend Snippet: rNurr1-V5 expression reduces sensorimotor deficits in parkinsonian rats. Rats were transfected with pTracer-rNurr1-V5 or pEGFP-N1 on day 30 post-BSSG lesion and evaluated 30 days after transfection (60 days post-BSSG lesion). (A, B) Time traveled (A) and number of errors per step (B) during displacement on a beam. (C, D) Ipsilateral (C) and contralateral (D) response to the vibrissae stimulation. (E) Asymmetry in discrimination of olfactory stimuli regularly distributed on each side of a corridor floor. (F) Asymmetry in the number of contacts of the forelimb paws on a transparent cylinder wall. Values are expressed as the mean ± SD of 6 independent rats for each experimental condition. * P < 0.05, healthy group vs . UT and pEGFP groups. One-way analysis of variance followed by Tukey's post hoc test was used. Healthy: rats without lesion; prNurr1: rats with BSSG lesion and transfected with pTracer-rNurr1-V5; pEGFP: rats with BSSG lesion and transfected with pEGFP-N1; UT: untransfected parkinsonian rats. BSSG: β-Sitosterol β-D-glucoside; ns: not significant.

Article Snippet: The Nurr1 sequence (1796 bp; GenBank, NM_019328; https://www.ncbi.nlm.nih.gov/search/all/?term=NM_019328) was obtained by a NheI-SpeI digestion from the prNurr1-DsRed2-N1 plasmid and subcloned between the SpeI restriction sites of the pTracer TM-EF/V5-His B plasmid (Invitrogen, Carlsbad, CA, USA).

Techniques: Expressing, Transfection