Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Query: UMLS:C0030567 (
Parkinson's disease
)
63,064
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Three neurodegenerative diseases [Amyotrophic Lateral Sclerosis (ALS),
Parkinson's disease
(PD) and Alzheimer's disease (AD)] have many characteristics like pathological mechanisms and genes. In this sense some researchers postulate that these diseases share the same alterations and that one alteration in a specific protein triggers one of these diseases. Analyses of gene expression may shed more light on how to discover pathways, pathologic mechanisms associated with the disease, biomarkers and potential therapeutic targets. In this review, we analyze four microarrays related to three neurodegenerative diseases. We will systematically examine seven genes (CHN1, MDH1, PCP4,
RTN1
, SLC14A1, SNAP25 and VSNL1) that are altered in the three neurodegenerative diseases. A network was built and used to identify pathways, miRNA and drugs associated with ALS, AD and PD using Cytoscape software an interaction network based on the protein interactions of these genes. The most important affected pathway is PI3K-Akt signalling. Thirteen microRNAs (miRNA-19B1, miRNA-107, miRNA-124-1, miRNA-124-2, miRNA-9-2, miRNA-29A, miRNA-9-3, miRNA-328, miRNA-19B2, miRNA-29B2, miRNA-124-3, miRNA-15A and miRNA-9-1) and four drugs (Estradiol, Acetaminophen, Resveratrol and Progesterone) for new possible treatments were identified.
...
PMID:Gene networks in neurodegenerative disorders. 2862 7
Reticulons (RTNs) are a group of membrane-bound proteins that are dominantly localized to the endoplasmic reticulum (ER).
RTN1
-C, one isoform of RTNs highly expressed in the brain, has been shown to mediate neuronal injury in cerebral ischemia models. The aim of this study was to investigate the role of
RTN1
-C in an in vitro model of
Parkinson's disease
(PD) mimicked by 1-methyl-4-phenylpyridinium (MPP
+
) treatment in SN4741 cells. We found that MPP
+
significantly increased the expression of
RTN1
-C, with no effect on
RTN1
-A and
RTN1
-B. Downregulation of
RTN1
-C using siRNA (Si-
RTN1
-C) markedly increased cell viability and inhibited apoptosis induced by MPP
+
treatment. The results of western blot showed that downregulation of
RTN1
-C inhibited the surface expression of metabotropic glutamate receptor 5 (mGluR5) but had no effect on mGluR1. The protective effects of Si-
RTN1
-C were partially prevented by activating mGluR5, not mGluR1. In addition, the results of Ca
2+
imaging showed that downregulation of
RTN1
-C attenuated intracellular Ca
2+
release induced by MPP
+
, which could be nullified by activation of mGluR5 pathway. In conclusion, our data suggest that downregulation of
RTN1
-C protects SN4741 cells against MPP
+
through mGluR5-mediated preservation of Ca
2+
homeostasis. Therefore,
RTN1
-C might represent a therapeutic target for the treatment of neuronal injury in experimental PD models.
...
PMID:Downregulation of RTN1-C attenuates MPP
+
-induced neuronal injury through inhibition of mGluR5 pathway in SN4741 cells. 3052 40
