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Valproic acid attenuates hyperglycemia induced complement and coagulation cascade gene expression

ABSTRACT: Valproic acid attenuates hyperglycemia induced complement and coagulation cascade gene expression

PROVIDER: PRJNA429757 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6467480.fastq.gz	Fastqsanger.gz
	SRR6467490.fastq.gz	Fastqsanger.gz
	SRR6467481.fastq.gz	Fastqsanger.gz
	SRR6467482.fastq.gz	Fastqsanger.gz
	SRR6467483.fastq.gz	Fastqsanger.gz

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Valproic acid attenuates hyperglycemia induced complement and coagulation cascade gene expression

Project description:Diabetes is a multifactorial disorder and epigenetics changes are increasingly appreciated to influence the development of diabetic complications. Chromatin remodeling and histone acetylation are implicated in activation of the inflammatory response. Recently, histone deacetylase (HDAC) inhibitors (HDACi) have proved to reduce the severity of inflammatory diseases. We have previously shown that chromatin alterations regulated by HDACi in HepG2 cells stimulated by hyperglycemia reduced hepatic glucose production. In this study, we examined gene expression patterns using next generation sequencing. We show the pharmacological HDAC inhibitor VPA attenuates hyperglycemia induced gene expression, highlighting the relevance of complement and coagulation cascade. These findings reveal a novel mechanism of VPA protection against hyperglycemia induced hepatic gene expression changes, which might improve the therapeutic approaches for diabetes.

2018-01-13 | GSE109140 | GEO

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Project description:A better understanding of the proteomic profile after bipolar disorder (BD) and schizophrenia (SCZ) treatment, through monitoring its progression, may assist the development of novel therapeutic strategies with the ability to reduce or control possible side effects. In this study, proteomics analysis employing liquid chromatography coupled to mass spectrometry (LC-MS) and bioinformatic tools were applied to identify differentially expressed proteins in serum of treated BD and SCZ patients. In total, 10 BD patients, 10 SCZ patients, and 14 healthy participants were included. From 25 serum proteins significantly altered (> 1.5- fold change), 8 were down-regulated in the BD group, while 7 proteins were up- regulated and 2 down-regulated in SCZ group when compared against healthy controls. Bioinformatics analysis based on these 25 proteins validated two main altered pathways previously described in the literature; furthermore, it revealed that opposite expressions of the complement and coagulation cascades were the most significant biological processes involved in these pathologies. Associations of disease-proteins and pathways suggest therapeutic intervention or prevention of comorbidities risks for BD and SCZ. Further validation and investigation are required to define whether there is correlation between complement and coagulation cascade expression for both diseases and cardiovascular diseases.

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Project description:IgE-binding monocytes upregulate the coagulation cascade in allergic horses

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Proteomics analysis of plasma-derived exosomes unveils the aberrant complement and coagulation cascades in dermatomyositis/polymyositis

Project description:Dermatomyositis and polymyositis (DM/PM) are systemic autoimmune diseases characterized by proximal muscle weakness. The underlying pathogenetic mechanism of this disease remains elusive. Here, using proteomics analysis, a great overlap of differentially expressed plasma exosomal proteins involved in the complement and coagulation cascades pathway, including FGA, FGB, FGG, C1QB, C1QC and VWF, were identified in DM/PM patients versus HCs. Correlation analysis revealed that the expression levels of complement-associated proteins (C1QB and C1QC) correlated positively with CRP, ESR and platelet count. ROC curve analysis demonstrated that complement and coagulation cascade-associated proteins could be strong predictors for DM/PM. Additionally, we also identified several other proteins that were differentially expressed in DM and PM, respectively. And the selected candidate proteins were further validated by PRM. Together, these exosome-derived proteins might participate in microvascular damage in DM/PM through the activation of the complement and coagulation cascades pathway and function as biomarkers for the clinical diagnosis of DM/PM.

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Proteomics analysis of plasma-derived exosomes unveils the aberrant complement and coagulation cascades in dermatomyositis/polymyositis

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Project description:IgE-binding monocytes are a rare peripheral immune cell type involved in the allergic response through binding of IgE on their surface. IgE-binding monocytes are present in both healthy and allergic individuals. We performed RNA sequencing to ask how the function of IgE-binding monocytes differs in the context of allergy. Using a large animal model of allergy, equine Culicoides hypersensitivity, we compared the transcriptome of IgE-binding monocytes in allergic and non-allergic horses at two seasonal timepoints: (i) when allergic animals were clinical healthy, in the winter “Remission Phase”, and (ii) during chronic disease, in the summer “Clinical Phase”. Most transcriptional differences between allergic and non-allergic horses occurred only during the “Remission Phase”, suggesting principal differences in monocyte function even in the absence of allergen exposure. F13A1, a subunit of fibrinoligase, was significantly upregulated at both timepoints in allergic horses. This suggested a role for increased fibrin deposition in the coagulation cascade to promote allergic inflammation. IgE-binding monocytes also downregulated CCR10 expression in allergic horses during the “Clinical Phase”, suggesting a defect in maintenance of skin homeostasis, which further promotes allergic inflammation. Together, this transcriptional analysis provides valuable clues into the mechanisms used by IgE-binding monocytes in allergic individuals.

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Proteomic analysis of lysine 2-hydroxyisobutyryl in SLE reveals protein modification alteration in Complement and coagulation cascades and Platelet activation pathways

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Valproic acid influences the expression of genes implicated with hyperglycaemia-induced complement and coagulation pathways.

Project description:Because the liver plays a major role in metabolic homeostasis and secretion of clotting factors and inflammatory innate immune proteins, there is interest in understanding the mechanisms of hepatic cell activation under hyperglycaemia and whether this can be attenuated pharmacologically. We have previously shown that hyperglycaemia stimulates major changes in chromatin organization and metabolism in hepatocytes, and that the histone deacetylase inhibitor valproic acid (VPA) is able to reverse some of these metabolic changes. In this study, we have used RNA-sequencing (RNA-seq) to investigate how VPA influences gene expression in hepatocytes. Interesting, we observed that VPA attenuates hyperglycaemia-induced activation of complement and coagulation cascade genes. We also observe that many of the gene activation events coincide with changes to histone acetylation at the promoter of these genes indicating that epigenetic regulation is involved in VPA action.

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