Integrated mRNA and miRNA expression profiling in blood reveals candidate biomarkers associated with endurance exercise in horse
Ontology highlight
ABSTRACT:
ORGANISM(S): Equus caballus
SUBMITTER: Nuria Mach
PROVIDER: E-GEOD-73104 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:The adaptive response to extreme endurance exercise might involve transcriptional and translational regulation by microRNAs (miRNAs). Therefore, the aim of this study was to define an integrative analysis of blood transcriptome and miRNome in horses before and after a long endurance ride (160 km) using equine microarrays. A total of 2,453 genes and 162 miRNAs were found to be differentially expressed (DEG) between animals at rest and after the endurance ride. To gain understanding of the biological functions regulated by the differentially expressed miRNA, we used a hypergeometric test analysis. Notably, we detected 42 differentially expressed miRNAs that putatively regulate a total of 350 depleted DEGs, involved in glucose metabolism, fatty acid oxidation, mitochondrion biogenesis, and immune response pathways. Graphical Gaussian models in an independent validation set of animals confirmed that 4 miRNAs could be strong candidate regulatory molecules for endurance exercise adaptation. This study represents, to the best of our knowledge, the first integrated comprehensive overview of the miRNA-mRNA co-regulation networks that may play a central role in controlling post-transcriptomic regulations during endurance exercise in horses. Sixty-one Arabian or half-breed Arabian horses (20 females and 41 geldings) aged 10 ± 2 years (±SEM) were recruited on voluntary basis of the owner on three 160 km endurance rides.
2016-09-04 | E-GEOD-73102 | biostudies-arrayexpress
Project description:The adaptive response to extreme endurance exercise might involve transcriptional and translational regulation by microRNAs (miRNAs). Therefore, the aim of this study was to define an integrative analysis of blood transcriptome and miRNome in horses before and after a long endurance ride (160 km) using equine microarrays. A total of 2,453 genes and 162 miRNAs were found to be differentially expressed (DEG) between animals at rest and after the endurance ride. To gain understanding of the biological functions regulated by the differentially expressed miRNA, we used a hypergeometric test analysis. Notably, we detected 42 differentially expressed miRNAs that putatively regulate a total of 350 depleted DEGs, involved in glucose metabolism, fatty acid oxidation, mitochondrion biogenesis, and immune response pathways. Graphical Gaussian models in an independent validation set of animals confirmed that 4 miRNAs could be strong candidate regulatory molecules for endurance exercise adaptation. This study represents, to the best of our knowledge, the first integrated comprehensive overview of the miRNA-mRNA co-regulation networks that may play a central role in controlling post-transcriptomic regulations during endurance exercise in horses. Sixty-one Arabian or half-breed Arabian horses (20 females and 41 geldings) aged 10 ± 2 years (±SEM) were recruited on voluntary basis of the owner on three 160 km endurance rides.
2016-09-04 | E-GEOD-72973 | biostudies-arrayexpress
Project description:MicroRNA expression levels in the lymphoblastic cells of prostate cancer patients and their healthy brothers from HPCX1 linked prostate cancer families were analyzed to trace variants that might alter miRNA expression and explain partly an inherited genetic predisposion to prostate cancer. MicroRNA expression levels in lymphoblastoid cell lines were detected using an Agilent Human miRNA V2 Oligo Microarray Kit (Agilent Technologies).100 ng of total RNA was used as a starting material, and miRNAs were labeled using the Agilent miRNA Labeling Kit. Labeled RNA was hybridized to Agilent miRNA arrays with eight identical arrays per slide, with each array containing probes directed against 723 human and 76 human viral miRNAs. Slides were scanned (Agilent microarray scanner) after hybridization and data was extracted using Feature Extraction software, version 9.5.1. (Agilent Technologies). Altogether 14 cancer patients and 15 healthy brothers from 11 families were included with no replicates.
2011-12-31 | E-GEOD-24201 | biostudies-arrayexpress
Project description:Defects in stress responses are important contributors in many chronic conditions including cancer, cardiovascular disease, diabetes, and obesity-driven pathologies like non-alcoholic steatohepatitis (NASH). Specifically, endoplasmic reticulum (ER) stress is linked with these pathologies and control of ER stress can ameliorate tissue damage. MicroRNAs have a critical role in regulating diverse stress responses including ER stress. Here we show that miR-494-3p plays a functional role during ER stress. ER stress inducers (tunicamycin and thapsigargin) robustly increase the expression of miR-494 in vitro in an ATF6 dependent manner. Surprisingly, miR-494 pretreatment dampens the induction and magnitude of ER stress in response to tunicamycin in endothelial cells. Conversely, inhibition of miR-494 increases ER stress de novo and amplifies the effects of ER stress inducers. Using Mass Spectrometry (TMT-MS) we identified many proteins that are downregulated by both tunicamycin and miR-494 in cultured human umbilical vein endothelial cells (HUVECs). Among these, we found 6 transcripts which harbor a putative miR-494 binding site. Our data indicates that ER stress driven miR-494 may act in a feedback inhibitory loop to dampen downstream ER stress signaling. We propose that RNA-based approaches targeting miR-494 or its targets may be attractive candidates for inhibiting ER stress dependent pathologies in human disease.
2021-09-09 | PXD019992 | Pride
Project description:MicroRNA plays a critical role in a wide variety of biological processes and regulate genes associated with different biological processes such as development, proliferation, apoptosis, stress response, and tumourigenesis. Profiling miRNA expression during differentiation of embryonic stem cells will help to understand the regulation pathway of differentiation, which in turn may elucidate disease mechanisms. In human hematopoiesis that requires a tight control of gene expression, lineage-specific transcription factors have long been known to act as key regulators of gene expression in multiple cell-fate decisions that govern cell differentiation. Given the important role of miRNAs in development and differentiation, it would be beneficial to elucidate the role of miRNAs in hematopoiesis for identifying novel drug targets. We undertook the current study of examining the expression of miRNA expression in CD34+ before and after differentiation into erythropoietic, granulopoietic and megakaryocytic cells using Affymetrix V 2.0 miRNA genechips. We identified 388 probesets representing 140 miRNAs, snoRNAs and stemloop RNAs to be significantly altered during lineage specific differentiation of CD34+ cells. Of these differentially expressed miRNAs with functional roles in cellular growth and proliferation, differentiation and apoptosis, 16 downregulated miRNAs were found to overlap between the E, M and G groups, hsa-miR150 was significantly downregulated and hsa-miR 210 and hsa-miR-1260b were found to be uniquely upregulated during granulopoiesis while hsa-miR486 was found to be upregulated during erythropoiesis and downregulated in megakaryopoiesis. Megakaryopoitic differentiation specifically resulted in significant down regulation of many miRNAs such as mir -150, mir -155, mir-15, mir-181, mir-221 that seem to play critical roles in the regulation of B and T cell differentiation . An integrated analysis of the differentially expressed miRNA and mRNA identified specific gene targets that are regulated by the significantly altered micro RNAs during lineage specific hematopoiesis. We believe that this study would enhance our understanding of the role of miRNA in lineage specific gene expression. CD34+ cells were compared to differentiated Erythropoitic, granulopoietic and megakaryopoiteic groups to identify differentially expressed microRNAs Human hematopoietic progenitor cells
2013-01-04 | E-GEOD-35532 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2011-12-31 | E-GEOD-24205 | biostudies-arrayexpress
Project description:We previously put forward a multi-layer systems toxicology framework for in vitro assessment of e-liquids that is meant to complement the battery of classical assays for genotoxicity testing. The framework started with the first layer to screen e-liquids for their potential toxicity, followed by the second layer to investigate the toxicity-related mechanism of a selected e-liquid(s), and finally the third layer to evaluate the toxicity-related mechanism of the corresponding aerosol(s). In this work, we leveraged this framework to assess the biological impact of an e-liquid MESH™ “Classic Tobacco” and its aerosol in comparison with the impact of 3R4F reference cigarettes. In the first layer, we evaluated the cytotoxicity profile of the MESH Classic Tobacco liquid (containing humectants, nicotine, and flavors) and its Base liquid (containing humectant and nicotine only) in comparison with total particulate matter (TPM) of 3R4F cigarette smoke (CS). In the second layer, we explored changes in specific markers using high content screening assays to identify potential toxicity-related mechanisms of the MESH Classic Tobacco and Base liquids beyond cell viability compared with the 3R4F TPM-induced effects. In the third layer, we compared the biological impact of exposure to the MESH Classic Tobacco aerosol with CS using human organotypic buccal and small airway epithelial cultures. The results showed that the cytotoxicity profile of the MESH Classic Tobacco liquid was similar to the Base liquid but lower than the toxicity of 3R4F TPM at comparable nicotine concentrations. When compared with CS exposure, MESH Classic Tobacco aerosol exposure did not cause tissue damage and elicited lower changes in the global mRNA, global microRNA, and protein markers. The global mRNA changes following Classic Tobacco aerosol exposure indicated perturbations in processes related to cell fate, cell stress, and inflammatory response that were less than 20% of the perturbations following CS exposure. In the context of tobacco-harm reduction strategy, the framework is suitable to assess the potential reduced impact of EC aerosol relative to CS.
2019-11-01 | E-MTAB-7912 | biostudies-arrayexpress
Project description:AIM: To investigate the molecular, structural, and functional impact of aerosols from two heat-not-burn-based MRTPs, the Carbon Heated Tobacco Product (CHTP) 1.2 and Tobacco Heating System (THS) 2.2, compared with that of cigarette mainstream smoke (CS) on the cardiovascular system of ApoE-/- mice. METHOD: Female ApoE-/- mice were exposed to aerosols from THS 2.2 and CHTP 1.2 or to CS from 3R4F for up to 6 months at matching nicotine concentrations. A cessation and a switching group (3 months exposure to 3R4F CS followed by filtered air or CHTP 1.2 for 3 months) were included. Cardiovascular effects were investigated using echocardiography, histopathology, immunohistochemistry, and transcriptomics. RESULTS: Continuous exposure to aerosols from CHTP 1.2 and THS 2.2 did not affect the atherosclerosis progression, heart function, left ventricular structure and cardiovascular transcriptome. Exposure to CS from 3R4F triggered atherosclerosis progression, reduced systolic ejection fraction and fractional shortening, caused heart left ventricle hypertrophy and initiated significant dysregulation in the transcriptomes of the heart ventricle and thoracic aorta. Importantly, smoking cessation and switching to CHTP 1.2 aerosol similarly improved the structural, functional, and molecular changes caused by 3R4F CS. CONCLUSION: Exposure to aerosols from CHTP 1.2 and THS 2.2 lacked most of the CS exposure-related functional, structural and molecular effects. Smoking cessation or switching to CHTP 1.2 aerosol caused a similar recovery from the 3R4F CS effect in the ApoE-/- model with no further acceleration of plaque progression beyond the aging-related rate.
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