Gene expression patterns for GDNF and its receptors in the human putamen affected by Parkinson's disease: A real-time PCR study

2006 ◽  
Vol 252 (1-2) ◽  
pp. 160-166 ◽  
Author(s):  
Cristina M. Bäckman ◽  
Lufei Shan ◽  
Ya Jun Zhang ◽  
Barry J. Hoffer ◽  
Sherry Leonard ◽  
...  
Keyword(s):  
Gene Expression ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Real Time ◽  
Real Time Pcr ◽  
Expression Patterns ◽  
Gene Expression Patterns

scholarly journals Microfluidic single-cell real-time PCR for comparative analysis of gene expression patterns

2012 ◽  
Vol 7 (5) ◽  
pp. 829-838 ◽  
Author(s):  
Veronica Sanchez-Freire ◽  
Antje D Ebert ◽  
Tomer Kalisky ◽  
Stephen R Quake ◽  
Joseph C Wu
Keyword(s):  
Gene Expression ◽  
Comparative Analysis ◽  
Single Cell ◽  
Real Time ◽  
Real Time Pcr ◽  
Expression Patterns ◽  
Gene Expression Patterns

scholarly journals Gene expression patterns in bone following lipopolysaccharide stimulation

2014 ◽  
Vol 19 (4) ◽  
Author(s):  
Jing Yang ◽  
Nan Su ◽  
Xiaolan Du ◽  
Lin Chen
Keyword(s):  
Gene Expression ◽  
Bone Formation ◽  
Real Time ◽  
Real Time Pcr ◽  
Early Stage ◽  
System Development ◽  
Expression Patterns ◽  
Osteoclast Differentiation ◽  
Gene Expression Patterns ◽  
Expression Levels

AbstractBone displays suppressed osteogenesis in inflammatory diseases such as sepsis and rheumatoid arthritis. However, the underlying mechanisms have not yet been clearly explained. To identify the gene expression patterns in the bone, we performed Affymetrix Mouse Genome 430 2.0 Array with RNA isolated from mouse femurs 4 h after lipopolysaccharide (LPS) administration. The gene expressions were confirmed with real-time PCR. The serum concentration of the N-terminal propeptide of type I collagen (PINP), a bone-formation marker, was determined using ELISA. A total of 1003 transcripts were upregulated and 159 transcripts were downregulated (more than twofold upregulation or downregulation). Increased expression levels of the inflammation-related genes interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor α (TNF-α) were confirmed from in the period 4 h to 72 h after LPS administration using real-time PCR. Gene ontogene analysis found four bone-related categories involved in four biological processes: system development, osteoclast differentiation, ossification and bone development. These processes involved 25 upregulated genes. In the KEGG database, we further analyzed the transforming growth factor β (TGF-β) pathway, which is strongly related to osteogenesis. The upregulated bone morphogenetic protein 2 (BMP2) and downregulated inhibitor of DNA binding 4 (Id4) expressions were further confirmed by real-time PCR after LPS stimulation. The osteoblast function was determined through examination of the expression levels of core binding factor 1 (Cbfa1) and osteocalcin (OC) in bone tissues and serum PINP from 4 h to 72 h after LPS administration. The expressions of OC and Cbfa1 decreased 6 h after administration (p < 0.05). Significantly suppressed PINP levels were observed in the later stage (from 8 h to 72 h, p < 0.05) but not in the early stage (4 h or 6 h, p > 0.05) of LPS stimulation. The results of this study suggest that LPS induces elevated expressions of skeletal system development- and osteoclast differentiation-related genes and inflammation genes at an early stage in the bone. The perturbed functions of these two groups of genes may lead to a faint change in osteogenesis at an early stage of LPS stimulation. Suppressed bone formation was found at later stages in response to LPS stimulation.

scholarly journals Transcriptomic signatures associated with regional cortical thickness changes in Parkinson’s disease

2020 ◽  
Author(s):  
Arlin Keo ◽  
Oleh Dzyubachyk ◽  
Jeroen van der Grond ◽  
Jacobus J. van Hilten ◽  
Marcel J. T. Reinders ◽  
...  
Keyword(s):  
Gene Expression ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cortical Thickness ◽  
Expression Patterns ◽  
Brain Atlas ◽  
Cortical Atrophy ◽  
Integrated Analysis ◽  
Gene Expression Patterns ◽  
Mitochondrial Translation

AbstractCortical atrophy is a common manifestation in Parkinson’s disease, particularly in later disease stages. Here, we investigated patterns of cortical thickness using T1-weighted anatomical MRI data of 149 Parkinson’s disease patients and 369 controls. To elucidate the molecular underpinnings of cortical thickness changes in Parkinson’s disease, we performed an integrated analysis of brain-wide healthy transcriptomic data from the Allen Human Brain Atlas and neuroimaging features. For this purpose, we used partial least squares regression to identify gene expression patterns correlated with cortical thickness changes. In addition, we identified gene expression patterns underlying the relationship between cortical thickness and clinical domains of Parkinson’s disease. Our results show that genes whose expression in the healthy brain is associated with cortical thickness changes in Parkinson’s disease are enriched in biological pathways related to sumoylation, regulation of mitotic cell cycle, mitochondrial translation, DNA damage responses, and ER-Golgi traffic. The associated pathways were highly related to each other and all belong to cellular maintenance mechanisms. The expression of genes within most pathways was negatively correlated with cortical thickness changes, showing higher expression in regions associated with decreased cortical thickness (atrophy). On the other hand, sumoylation pathways were positively correlated with cortical thickness changes, showing higher expression in regions with increased cortical thickness (hypertrophy). Our findings suggest that alterations in the balanced interplay of these mechanisms play a role in changes of cortical thickness in Parkinson’s disease and possibly influence motor and cognitive functions.

Contrasting gene expression patterns induced by levodopa and pramipexole treatments in the rat model of Parkinson's disease

2016 ◽  
Vol 101 ◽  
pp. 576-589 ◽  
Author(s):  
Irene R. Taravini ◽  
Celia Larramendy ◽  
Gimena Gomez ◽  
Mariano D. Saborido ◽  
Floor Spaans ◽  
...  
Keyword(s):  
Gene Expression ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Rat Model ◽  
Expression Patterns ◽  
Gene Expression Patterns

scholarly journals Transcriptomic Signatures Associated With Regional Cortical Thickness Changes in Parkinson’s Disease

2021 ◽  
Vol 15 ◽  
Author(s):  
Arlin Keo ◽  
Oleh Dzyubachyk ◽  
Jeroen van der Grond ◽  
Jacobus J. van Hilten ◽  
Marcel J. T. Reinders ◽  
...  
Keyword(s):  
Gene Expression ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cortical Thickness ◽  
Expression Patterns ◽  
Brain Atlas ◽  
Cortical Atrophy ◽  
Integrated Analysis ◽  
Gene Expression Patterns ◽  
Mitochondrial Translation

Cortical atrophy is a common manifestation in Parkinson’s disease (PD), particularly in advanced stages of the disease. To elucidate the molecular underpinnings of cortical thickness changes in PD, we performed an integrated analysis of brain-wide healthy transcriptomic data from the Allen Human Brain Atlas and patterns of cortical thickness based on T1-weighted anatomical MRI data of 149 PD patients and 369 controls. For this purpose, we used partial least squares regression to identify gene expression patterns correlated with cortical thickness changes. In addition, we identified gene expression patterns underlying the relationship between cortical thickness and clinical domains of PD. Our results show that genes whose expression in the healthy brain is associated with cortical thickness changes in PD are enriched in biological pathways related to sumoylation, regulation of mitotic cell cycle, mitochondrial translation, DNA damage responses, and ER-Golgi traffic. The associated pathways were highly related to each other and all belong to cellular maintenance mechanisms. The expression of genes within most pathways was negatively correlated with cortical thickness changes, showing higher expression in regions associated with decreased cortical thickness (atrophy). On the other hand, sumoylation pathways were positively correlated with cortical thickness changes, showing higher expression in regions with increased cortical thickness (hypertrophy). Our findings suggest that alterations in the balanced interplay of these mechanisms play a role in changes of cortical thickness in PD and possibly influence motor and cognitive functions.

Comparison Analysis of Gene Expression Patterns between Sporadic Alzheimer's and Parkinson's Disease

2007 ◽  
Vol 12 (4) ◽  
pp. 291-311 ◽  
Author(s):  
Edna Grünblatt ◽  
Nicole Zander ◽  
Jasmin Bartl ◽  
Li Jie ◽  
Camelia-Maria Monoranu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Expression Patterns ◽  
Gene Expression Patterns ◽  
Comparison Analysis

scholarly journals Interpreting the dynamic pathogenesis of Parkinson’s disease by longitudinal blood transcriptome analysis

2020 ◽  
Author(s):  
Gang Xue ◽  
Gang Wang ◽  
Qianqian Shi ◽  
Hui Wang ◽  
Bo-Min Lv ◽  
...  
Keyword(s):  
Gene Expression ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Stem Cell ◽  
Transcriptome Analysis ◽  
Expression Patterns ◽  
Gene Expression Patterns ◽  
Prodromal Phase ◽  
Stem Cell Pluripotency ◽  
Blood Transcriptome

AbstractAchieving an improved understanding of the temporal sequence of factors involved in Parkinson’s disease (PD) pathogenesis may accelerate drug discovery. In this study, we performed a longitudinal transcriptome analysis to identify associated genes underlying the pathogenesis of PD at three temporal phases. We firstly found that multiple initiator genes, which are related to processes of olfactory transduction and stem cell pluripotency, indicate PD risk to those subjects at the prodromal phase. And many facilitator genes involved in calcium signaling and stem cell pluripotency contribute to PD onset. We next identified 325 aggravator genes whose expression could lead to disease progression through damage to dopaminergic synapses and ferroptosis via an integrative analysis with DNA methylation. Last, we made a systematic comparison of gene expression patterns across PD development and accordingly provided candidate drugs at different phases in an attempt to prevent the neurodegeneration process.

scholarly journals C. elegans genetic background modifies the core transcriptional response in an α-synuclein model of Parkinson’s disease

2018 ◽  
Author(s):  
Yiru A. Wang ◽  
Basten L. Snoek ◽  
Mark G. Sterken ◽  
Joost A.G. Riksen ◽  
Jana J. Stastna ◽  
...  
Keyword(s):  
Gene Expression ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Genetic Background ◽  
Expression Patterns ◽  
Transcriptional Response ◽  
Global Gene Expression ◽  
C Elegans ◽  
The Core ◽  
Repair Mechanisms

AbstractAccumulation of protein aggregates is a major cause of Parkinson’s disease (PD), a progressive neurodegenerative condition that is one of the most common causes of dementia. Transgenic Caenorhabditis elegans worms expressing the human synaptic protein α-synuclein show inclusions of aggregated protein and replicate the defining pathological hallmarks of PD. It is however not known how PD progression and pathology differs among individual genetic backgrounds. Here, we compared gene expression patterns, and investigated the phenotypic consequences of transgenic α-synuclein expression in five different C. elegans genetic backgrounds. Transcriptome analysis indicates that the effects of -synuclein expression on pathways associated with nutrient storage, lipid transportation and ion exchange depend on the genetic background. The gene expression changes we observe suggest that a range of phenotypes will be affected by α-synuclein expression. We experimentally confirm this, showing that the transgenic lines generally show delayed development, reduced lifespan, and an increased rate of matricidal hatching. These phenotypic effects coincide with the core changes in gene expression, linking developmental arrest, mobility, metabolic and cellular repair mechanisms to α-synuclein expression. Together, our results show both genotype-specific effects and core alterations in global gene expression and in phenotype in response to -synuclein. We conclude that the PD effects are substantially modified by the genetic background, illustrating that genetic background mechanisms should be elucidated to understand individual variation in PD.

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