Gene expression data from brain striatal and spinal cord regions of MPTP-intoxicated mouse following acupuncture
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ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Sabina Lim
PROVIDER: E-GEOD-24838 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Acupuncture at acupoints GB34 and LR3 has been reported to inhibit nigrostriatal degeneration in parkinsonism models, yet the genes related to this preventive effect of acupuncture on the nigrostriatal dopaminergic system remain elusive. We investigated gene expression profile changes in the striatal region of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism models after acupuncture at the acupoints GB34 and LR3 C57BL/6 mice were divided into four experimental groups; â C: Control, â¡ M: MPTP-treatment only, ⢠MA: MPTP- and acupuncture-treatment at acupoints GB34 and LR3, ⣠MNA: MPTP- and acupuncture-treatment at non-acupoints. Total RNA was isolated from two brains' striatal regions of each experimental group (4 experimental group à 2 samples of each experimental group = total 8 samples).
2010-10-23 | E-GEOD-24829 | biostudies-arrayexpress
Project description:It has been shown that acupuncture at acupoints GB34 and LR3 inhibits the degeneration of nigrostriatal neurons in an 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinsonâ??s disease. This preventative effect of peripheral acupuncture stimulation is hypothesized to be transmitted through the spinal cord to the nigrostriatal neurons. The gene expression profile changes following acupuncture at the acupoints were investigated in the cervical spinal cord of an MPTP-induced parkinsonism model using an Affymetrix genechip mouse gene 1.0 ST array. C57BL/6 mice were divided into four experimental groups; â? C: Control, â?¡ M: MPTP-treatment only, â?¢ MA: MPTP- and acupuncture-treatment at acupoints GB34 and LR3, â?£ MNA: MPTP- and acupuncture-treatment at non-acupoints. Total RNA was isolated from the cervical spinal cord regions of each experimental group (4 experimental group Ã? 2 samples of each experimental group = total 8 samples).
2010-10-23 | E-GEOD-24830 | biostudies-arrayexpress
Project description:Acupuncture stimulations at GB34 and LR3 inhibit the reduction of tyrosine hydroxylase in the nigrostriatal dopaminergic neurons in the parkinsonism animal models. Especially, behavioral tests showed that acupuncture stimulations improved the motor dysfunction in a previous study. The thalamus is a crucial area for the motor circuit and has been identified as one of the most markedly damaged areas in Parkinson’s disease (PD), so acupuncture stimulations might also have an effect on the thalamic damage. We investigated gene expression profile changes in the thalamic region of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism models after acupuncture at the acupoints GB34 and LR3 C57BL/6 mice were divided into four experimental groups; ① C: Control, ② M: MPTP-treatment only, ③ MA: MPTP- and acupuncture-treatment at acupoints GB34 and LR3, ④ MNA: MPTP- and acupuncture-treatment at non-acupoints. Total RNA was isolated from two brains' thalamic regions of each experimental group (4 experimental group × 2 samples of each experimental group = total 8 samples).
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Project description:To characterize both short- and long-term (7 days and 28 days) gene expression profiling differences between control and MPTP-treated retina, we determined levels of gene expression using microarray analysis and real-time PCR. We found 60 genes relatively regulated in retinas treated with MPTP for 7 days (26 up-regulated and 34 down-regulated), whereas 54 genes were regulated in retinas treated with MPTP for 28 days (18 up-regulated and 36 down-regulated) when compared with the non-treated retina in each control groups. Total 26 annotated differently expressed genes were chosen for further validation by quantitative real-time PCR, and 4 genes in the 7-day treatment group (Clec2e; Dio2; Hmcn1; Rlbp1) and 3 genes in the 28-days treatment group (Pnmt; Tmem121; Ssxb3) were confirmed. Male C57BL/6 mice were randomly divided into four treatment groups (n= 6 in each group): the 7 days and 28 days saline-injection (control) groups (C-7 and C-28, respectively), and 7 days and 28 days MPTP-injection groups (M-7 and M-28, respectively). 4 retinas for 1 samples (1 gene chip), (4 experimental group × 2 samples of each experimental group = total 8 samples).
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Project description:In Parkinsonâ??s disease (PD), the progressive loss of substantia nigra dopamine cells has been associated with their vulnerability to oxidative stress, inflammation, and mitochondrial dysfunction. To identify multiple gene transcription alterations that may potentially underlie early stages of related degenerative processes in brain, we used the subcrhonic MPTP mouse model of PD and microarray analysis at 4 days post-MPTP when neurotoxic activity is maximal. Since PD results in gene changes throughout the brain, we assessed MPTP's effects in multiple regions: frontal cortex, striatum and midbrain. Experiment Overall Design: Mus musculus adults were randomly assigned to either MPTP or saline treatment groups. Brain regions of interest (frontal cortex, striatum and midbrain) were dissected from both groups for RNA extraction and hybridization on Affymetrix microarrays.
2008-10-26 | E-GEOD-7707 | biostudies-arrayexpress
Project description:PD is the second most common neurodegenerative disease worldwide with growing prevalence. MPTP is a neurotoxin which causes the appearance of Parkinson's disease (PD) pathology. The involvement of the cholinergic system in PD has been identified decades ago and anti-cholinergic drugs were upon the first drugs used for symptomatic treatment of PD. Of note, MPTP intoxication is a model of choice for symptomatic neuroprotective therapies since it have been quite predictive. Mice were exposed to the dopaminergic neurotoxin 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP), with or without the protective acetylcholinesterase (AChE-R) variant. Transgenic AChE-S (the synaptic variant), AChE-R (the shorter, protective variant) and FVB/N control mice were included in this study. Two brain regions were examined: the pre-frontal cortex (PFC) and the striatal caudate-putamen (CPu). Each condition (i.e brain region and transgenic variant) was examined on both naive and MPTP-exposed mice. 29 microarrays including hybridizations of control FVB/N PFC, control FVB/N CPu,control S transgenics PFC, control S transgenics CPu, control R transgenics PFC, control R transgenice CPu, MPTP FVB/N PFC, MPTP FVB/N CPu, MPTP S transgenics PFC, MPTP S transgenics CPu, MPTP R transgenics PFC and MPTP R transgenice CPu mRNA.
2012-01-09 | E-GEOD-31458 | biostudies-arrayexpress
Project description:We characterized the transcriptomic profiles of cells from the substantia nigra (SN) of mice with co-injection with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and selective inhibitor of GCase activity (conduritol-β-epoxide, (CBE)) to mimic PD bearing GCase dysfunction (MPTP+CBE), mice treated with MPTP, mice treated with CBE and control mice treated with injec-tion of sodium chloride (NaCl) (vehicle).
2023-08-31 | E-MTAB-13244 | biostudies-arrayexpress
Project description:Implications for neuroprotection in Parkinson's disease Parkinson’s disease and its characteristic symptoms are thought to arise from the progressive degeneration of specific midbrain dopamine (DA) neurons. In humans, DA neurons of the substantia nigra (SN) and their projections to the striatum show selective vulnerability, while neighboring DA neurons of the ventral tegmental area (VTA) are relatively spared from degeneration. This pattern of cell loss is mimicked in humans, primates, and certain rodents by the neurotoxin MPTP. In this study, we aimed to test the hypothesis that there are factors in the VTA that are potentially neuroprotective against MPTP and that these factors change over time. We have found a differential transcriptional response within the cells of the SN and VTA to sustained exposure to a low dose of MPTP. Specifically, the VTA has increased expression of 148 genes as an early response to MPTP and 113 genes as a late response to MPTP toxicity. This response encompasses many areas of cellular function, including protein regulation (Phf6) and ion/metal regulation (PANK2, Car4). Notably, these responses were largely absent from the cells of the SN. Our data show a clear dynamic response in maintaining the homeostasis and viability of the neurons in the VTA that is lacking in the SN after neurotoxin challenge. We used microarrays to analyze the differential response of the substantia nigra (SN) and ventral tegmental area (VTA) to a chronic low dose of the neurotoxin MPTP. Transgenic hTH-GFP mice were treated with MPTP (4mg/kg) for either 2 or 10 days. Control mice were given an equal volume of saline for 10 days. Dopamine neurons from the substantia nigra and ventral tegmental areas of control and MPTP treated animals were laser captured. The RNA was isolated and processed for microarray hybridization. Each group had three biological replicates, for a total of 18 samples. Three each in the following: Control SN, Control VTA, 2 day MPTP SN, 2 day MPTP VTA, 10 day MPTP SN, 10 day MPTP VTA. Samples were log2 transformed and RMA normalized using Agilent Genespring 10.0 GX.
2009-12-31 | E-GEOD-17542 | biostudies-arrayexpress
Project description:Gene expression data from striatal regions of MPTP-intoxicated mouse brain by acupuncture
| PRJNA133423 | ENA
Project description:Gene expression data from thalamic regions of MPTP-intoxicated mouse brain by acupuncture
| PRJNA150819 | ENA