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Multi-species transcriptomic data analysis reveal three candidate genes, responsible for the transition from compensated left ventricle hypertrophy to heart failure
Session:
CO 05 - Ciência Básica
Speaker:
Mónica Abreu
Congress:
CPC 2021
Topic:
O. Basic Science
Theme:
36. Basic Science
Subtheme:
36.3 Basic Science - Cardiac Diseases
Session Type:
Comunicações Orais
FP Number:
---
Authors:
Mónica Abreu; Cátia Ferreira; Lino Gonçalves; Henrique Girão; Rui Baptista
Abstract
<p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif">Introduction:</span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif">Heart failure (HF) is the common final syndrome for a wide spectrum of heart diseases, including hypertrophic cardiomyopathy, systemic arterial hypertension, aortic stenosis and aortic coarctation, usually following a variable period of compensated left ventricle hypertrophy (cLVH). Despite its importance, the transition from a cLVH phenotype to overt HF in humans is poorly understood. In this study, we aimed to find a molecular signature for the transition from cLVH to decompensated HF conserved among species and mechanisms of disease.</span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif">Methods:</span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif">Four datasets, containing gene expression data of cLVH and HF samples, were selected from GEO data repository. The selected datasets included three different species: <em>Rattus norvegicus </em>(GSE4286 and GSE47495), <em>Canis lupus familiaris</em> (GSE5247) and <em>Cavia porcellus</em> (GSE78077) and different models of cLVH (pressure overload, genetic, and both). The intensity files (CEL files) containing the expression data were analysed using the Transcriptome Analysis Console 4.0 (TAC 4.0.2.15, Applied Biosystems). To identify differentially expressed genes (DEGs) a p-value cutoff of 0.05 was applied.</span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif">Results:</span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif">The lists of DEGs obtained in the comparison cLVH <em>versus</em> HF, in each dataset, were uniformized to human identifiers and merged, resulting in a list containing 8307 genes. Most of the genes were differentially expressed in only one dataset (6252, 75.3%). DEGs present in two datasets were 1850 (22.3%), in three datasets 202 (2.4%), and finally, present in all datasets only 3 genes were found. The first gene identified was CDKS1B (<span style="background-color:white"><span style="color:black">CDK regulatory protein)</span></span>, which belongs to a family of proteases related to the cell cycle. CKS1B upregulation activates the STAT3 and MEK/ERK pathways and promotes cell proliferation. Indeed, negative regulation of the MEK/ERK reduces cardiac hypertrophy induced by pressure overload. Secondly, type 2 phosphatidylinositol-5-phosphate 4-kinase (PI5P4K) converts phosphatidylinositol-5-phosphate to phosphatidylinositol-4,5-bisphosphate, and plays an important role in inflammatory response and autophagy. However, its role in the heart remains unknow. Lastly, the Mesenteric Estrogen Dependent Adipogenesis (MEDAG) adipokine was also differentially expressed in HF. Its role in myocyte metabolism is not defined but may parallel nutrient uptake role seen in adipose and reflect reliance on lipid oxidation.</span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif"><span style="background-color:white"><span style="color:#212121">Conclusions:</span></span></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Calibri,sans-serif">We identified three genes that are differentially expressed in HF compared to cLVH, involved in cell proliferation, autophagy, inflammation, and lipid metabolism. This data requires confirmation in human studies. Such advance would be an important step toward identifying those risk factors, especially genetic variation, that predispose individuals with cLVH to develop HF.</span></span></p>
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