scholarly journals Differential Gene Expression Reveals Mitochondrial Dysfunction in an Imprinting Center Deletion Mouse Model of Prader-Willi Syndrome

2013 ◽  
Vol 6 (5) ◽  
pp. 347-355 ◽  
Author(s):  
Puya G. Yazdi ◽  
Hailing Su ◽  
Svetlana Ghimbovschi ◽  
Weiwei Fan ◽  
Pinar E. Coskun ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mouse Model ◽  
Mitochondrial Dysfunction ◽  
Differential Gene Expression ◽  
Prader Willi Syndrome ◽  
Imprinting Center ◽  
Differential Gene

scholarly journals Comparative RNA-sequencing profiled the differential gene expression of liver in response to acetyl-CoA carboxylase inhibitor GS-0976 in a mouse model of NASH

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e8115
Author(s):  
Ying Lu ◽  
Xiaolan Su ◽  
Manyu Zhao ◽  
Qianru Zhang ◽  
Chuang Liu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mouse Model ◽  
Rna Sequencing ◽  
Hepatic Steatosis ◽  
Differential Gene Expression ◽  
Receptor Interaction ◽  
Therapeutic Effects ◽  
Acetyl Coa Carboxylase ◽  
Acetyl Coa ◽  
Differential Gene

Background Non-alcoholic steatohepatitis (NASH) is a progressive liver disease characterized by hepatic steatosis, lobular inflammation and fibrosis. Acetyl-CoA carboxylase (ACC) isoform 1 and 2 involved in de novo lipogenesis (DNL) and fatty acid oxidation have been identified as a therapeutic target in NASH. GS-0976, the inhibitor of ACC1 and ACC2, has achieved favorable therapeutic effects in clinical trials with NASH. The purpose of this study was to explore the transcriptional alterations regulated by GS-0976 in NASH. Methods C57BL/6 mice were fed on a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) or normal diet for 12 weeks. Mice were treated with or without GS-0976 (3 mg/kg per day) in the last 8 weeks. Oil Red O, Haematoxylin-eosin (H & E), and Sirius Red were used to evaluate hepatic steatosis, inflammation and fibrosis. The comparative RNA-sequencing was conducted to analyse the hepatic gene expression profiles in mice. Reverse transcription–polymerase chain reaction analysis was performed to validate the differential expression of representative genes. Results GS-0976 attenuated the steatosis, inflammation, and fibrosis of NASH in CDAHFD mouse model. High-throughput sequencing and differential gene expression analysis showed that there were 516 up-regulated genes and 525 down-regulated genes after GS-0976 treatment. Genes involved in the metabolic process, extracellular matrix formation, immune response, and angiogenesis were significantly enriched. The “Metabolic pathways” and “ECM-receptor interaction” pathways were the most significantly enriched KEGG pathways in the up-regulated and down-regulated differentially expressed genes (DEGs), respectively. Conclusions Transcriptome analysis showed that GS-0976 could regulate the expression of genes related to metabolism, inflammation and fibrosis in NASH. The global transcriptomic changes in gene expression promote the further understanding for the inhibition mechanisms of GS-0976 in NASH.

scholarly journals Whole genome microarray analysis of gene expression in an imprinting center deletion mouse model of Prader–Willi syndrome

2007 ◽  
Vol 143A (5) ◽  
pp. 422-429 ◽  
Author(s):  
Douglas C. Bittel ◽  
Nataliya Kibiryeva ◽  
Steven G. McNulty ◽  
Daniel J. Driscoll ◽  
Merlin G. Butler ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mouse Model ◽  
Microarray Analysis ◽  
Prader Willi Syndrome ◽  
Whole Genome ◽  
Imprinting Center ◽  
Whole Genome Microarray

scholarly journals Upregulated Ribosomal Pathway Impairs Follicle Development in a Polycystic Ovary Syndrome Mouse Model: Findings of Differential Gene Expression Analysis of Oocytes

2021 ◽  
Author(s):  
Natsuki Nakanishi ◽  
Satoko Osuka ◽  
Tomohiro Kono ◽  
Hisato Kobayashi ◽  
Shinya Ikeda ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Mouse Model ◽  
Differential Gene Expression ◽  
Polycystic Ovary ◽  
Methylation Status ◽  
Rna Seq ◽  
Ovary Syndrome ◽  
Pcos Group ◽  
Differential Gene

Abstract Background: Polycystic ovary syndrome (PCOS), a common endocrinal disorder, is associated with impaired oocyte development, which leads to infertility. However, the pathogenesis of PCOS has not been completely elucidated. Limited studies have analyzed the pathological characteristics of oocytes in PCOS. This study aimed to analyze the differentially expressed genes (DEGs) and epigenetic changes in the oocytes of the PCOS mouse model to identify the etiological factors.Methods: C57BL/6J female mice were subcutaneously injected with vehicle or 5α-dihydrotestosterone (250 µg/day) on days 16–18 of pregnancy. Female offspring were used as the control or PCOS group. The oocytes were collected from mice aged 7–9 weeks. The DEGs between the control and PCOS groups were analyzed using RNA sequencing (RNA-Seq). Additionally, the DNA methylation status was analyzed using the post-bisulfite adaptor tagging method. The ovarian tissue sections were stained with hematoxylin and eosin to examine the morphological changes. The proteins, Rps21 and Rpl36, were measured using immunostaining.Results: Compared with the control group, the PCOS group exhibited impaired estrous cycle and polycystic ovary-like morphology. RNA-Seq analysis revealed that 90 DEGs were upregulated and 27 DEGs were downregulated in the PCOS mouse model. DNA methylation analysis revealed 30 hypomethylated and 10 hypermethylated regions in the PCOS group. However, the DNA methylation status was not correlated with differential gene expression. The Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis revealed that five DEGs (Rps21, Rpl36, Rpl36a, Rpl37a, and Rpl22l1) were enriched in ribosome-related pathways. The immunohistochemical analysis revealed that the expression levels of Rps21 and Rpl36 were significantly upregulated in the PCOS mouse model.Conclusions: These results suggest that differential gene expression in the oocytes of the PCOS mouse model is related to impaired folliculogenesis. These findings improved our understanding of the pathogenesis of PCOS.

scholarly journals Studying the differential gene expression patterns of Hippocampus and Amygdala associated with social stress in mouse model

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
seshamalini srinivasan ◽  
Bintu Sowe ◽  
Stacy-Ann Miller ◽  
Seid Muhie ◽  
Nabarun Chakraborty ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mouse Model ◽  
Differential Gene Expression ◽  
Social Stress ◽  
Expression Patterns ◽  
Gene Expression Patterns ◽  
Differential Gene

scholarly journals INPP5D Expression is Associated with Risk for Alzheimer’s Disease and Induced by Plaque-Associated Microglia

2020 ◽  
Author(s):  
Andy P Tsai ◽  
Peter Bor-Chian Lin ◽  
Chuanpeng Dong ◽  
Miguel Moutinho ◽  
Brad Casali ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Differential Gene Expression ◽  
Expression Analysis ◽  
Gene Expression Analysis ◽  
Differential Gene Expression Analysis ◽  
Differential Gene ◽  
5Xfad Mice

Abstract Background Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, robust microgliosis, neuroinflammation, and neuronal loss. Genome-wide association studies recently highlighted a prominent role for microglia in late-onset AD (LOAD). Specifically, inositol polyphosphate-5-phosphatase (INPP5D), also known as SHIP1, is selectively expressed in brain microglia and has been reported to be associated with LOAD. Although INPP5D is likely a crucial player in AD pathophysiology, its role in disease onset and progression remains unclear. Methods We performed differential gene expression analysis to investigate INPP5D expression in LOAD and its association with plaque density and microglial markers using transcriptomic (RNA-Seq) data from the Accelerating Medicines Partnership for Alzheimer’s Disease (AMP-AD) cohort. We also performed quantitative real-time PCR, immunoblotting, and immunofluorescence assays to assess INPP5D expression in the 5xFAD amyloid mouse model. Results Differential gene expression analysis found that INPP5D expression was upregulated in LOAD and positively correlated with amyloid plaque density. In addition, in 5xFAD mice, Inpp5d expression increased as the disease progressed, and selectively in plaque-associated microglia. Increased Inpp5d expression levels in 5xFAD mice were abolished entirely by depleting microglia with the colony-stimulating factor receptor-1 antagonist PLX5622. Conclusions Our findings show that INPP5D expression increases as AD progresses, predominantly in plaque-associated microglia. Importantly, we provide the first evidence that increased INPP5D expression might be a risk factor in AD, highlighting INPP5D as a potential therapeutic target. Moreover, we have shown that the 5xFAD mouse model is appropriate for studying INPP5D in AD.

scholarly journals INPP5D expression is associated with risk for Alzheimer’s disease and induced by plaque-associated microglia

2020 ◽  
Author(s):  
Andy P. Tsai ◽  
Peter Bor-Chian Lin ◽  
Chuanpeng Dong ◽  
Miguel Moutinho ◽  
Brad T. Casali ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Differential Gene Expression ◽  
Expression Analysis ◽  
Gene Expression Analysis ◽  
Differential Gene Expression Analysis ◽  
Differential Gene ◽  
5Xfad Mice

AbstractBackgroundAlzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, robust microgliosis, neuroinflammation, and neuronal loss. Genome-wide association studies recently highlighted a prominent role for microglia in late-onset AD (LOAD). Specifically, inositol polyphosphate-5-phosphatase (INPP5D), also known as SHIP1, is selectively expressed in brain microglia and has been reported to be associated with LOAD. Although INPP5D is likely a crucial player in AD pathophysiology, its role in disease onset and progression remains unclear.MethodsWe performed differential gene expression analysis to investigate INPP5D expression in LOAD and its association with plaque density and microglial markers using transcriptomic (RNA-Seq) data from the Accelerating Medicines Partnership for Alzheimer’s Disease (AMP-AD) cohort. We also performed quantitative real-time PCR, immunoblotting, and immunofluorescence assays to assess INPP5D expression in the 5xFAD amyloid mouse model.ResultsDifferential gene expression analysis found that INPP5D expression was upregulated in LOAD and positively correlated with amyloid plaque density. In addition, in 5xFAD mice, Inpp5d expression increased as the disease progressed, and selectively in plaque-associated microglia. Increased Inpp5d expression levels in 5xFAD mice were abolished entirely by depleting microglia with the colony-stimulating factor receptor-1 antagonist PLX5622.ConclusionsOur findings show that INPP5D expression increases as AD progresses, predominantly in plaque-associated microglia. Importantly, we provide the first evidence that increased INPP5D expression might be a risk factor in AD, highlighting INPP5D as a potential therapeutic target. Moreover, we have shown that the 5xFAD mouse model is appropriate for studying INPP5D in AD.

scholarly journals Differential gene expression between skin and cervix induced by the E7 oncoprotein in a transgenic mouse model

Virology ◽  
2012 ◽  
Vol 433 (2) ◽  
pp. 337-345 ◽  
Author(s):  
E. Ibarra Sierra ◽  
J. Díaz Chávez ◽  
E.M. Cortés-Malagón ◽  
L. Uribe-Figueroa ◽  
A. Hidalgo-Miranda ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Differential Gene Expression ◽  
Transgenic Mouse Model ◽  
E7 Oncoprotein ◽  
Differential Gene

scholarly journals Differential Gene Expression Analysis of Oocytes in a PCOS Mouse Model Revealed the Relation of Ribosomal Pathway

2022 ◽  
Author(s):  
Natsuki Nakanishi ◽  
Satoko Osuka ◽  
Tomohiro Kono ◽  
Hisato Kobayashi ◽  
Shinya Ikeda ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Mouse Model ◽  
Differential Gene Expression ◽  
Polycystic Ovary ◽  
Methylation Status ◽  
Immunohistochemical Analysis ◽  
Pathway Enrichment Analysis ◽  
Sequencing Analysis ◽  
Differential Gene

Abstract Polycystic ovary syndrome (PCOS), a common endocrinal disorder, is associated with impaired oocyte development, which leads to infertility. However, the pathogenesis of PCOS has not been completely elucidated. This study aimed to analyze the differentially expressed genes (DEGs) and epigenetic changes in the oocytes of the PCOS mouse model to identify the etiological factors. In this study, RNA-sequencing analysis revealed that 90 DEGs were upregulated and 27 DEGs were downregulated in the PCOS mouse model. DNA methylation analysis revealed 30 hypomethylated and 10 hypermethylated regions in the PCOS group. However, the DNA methylation status was not correlated with differential gene expression. The pathway enrichment analysis revealed that five DEGs (Rps21, Rpl36, Rpl36a, Rpl37a, and Rpl22l1) were enriched in ribosome-related pathways in the oocytes of the PCOS mouse model, and the immunohistochemical analysis revealed significantly upregulated expression levels of Rps21 and Rpl36. These results suggest that differential gene expression in the oocytes of the PCOS mouse model is related to impaired folliculogenesis. These findings improved our understanding of the pathogenesis of PCOS.

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