Identification of miRNA-mRNA regulatory network for Human Atrial Aging [mRNA]
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE136928 | GEO | 2019/09/06
REPOSITORIES: GEO
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Project description:We report an integrative analysis of miRNA-seq and mRNA-seq to identify miRNAs, genes, and miRNA-mRNA interactions for human atrial aging (AA). We found that seven miRNAs (4 upregulation and 3 downregulation) and 42 genes (23 upregulation and 19 downregulation) show differential expression between older samples and younger samples in human right atrial tissues. Pearson correlation analysis identified 114 pairs of putative miRNA-mRNA interactions for AA. Pathway enrichment analysis identified three important pathways including rhythmic process, senescence and autophagy in cancer, and positive regulation of cytokine biosynthetic process. Our study revealed novel miRNA-mRNA interaction networks and signaling pathways for AA, providing novel insights into the development of human AA. This dataset includes data generation and processing steps for the miRNA-seq data generated from twelve SR samples.
2019-09-06 | GSE136926 | GEO
Project description:As the fetal heart develops, cardiomyocyte proliferation potential decreases while fatty acid oxidative capacity increases, a highly regulated transition known as cardiac maturation. Small noncoding RNAs, such as microRNAs (miRNAs), contribute to the establishment and control of tissue-specific transcriptional programs. However, small RNA expression dynamics and genome wide miRNA regulatory networks controlling maturation of the human fetal heart remain poorly understood. Transcriptome profiling of small RNAs revealed the temporal expression patterns of miRNA, piRNA, circRNA, snoRNA, snRNA and tRNA in the developing human heart between 8 and 19 weeks of gestation. Our analysis revealed that miRNAs were the most dynamically expressed small RNA species throughout mid-gestation. Cross-referencing differentially expressed miRNAs and mRNAs predicted 6,200 mRNA targets, 2134 of which were upregulated and 4066 downregulated as gestation progresses. Moreover, we found that downregulated targets of upregulated miRNAs predominantly control cell cycle progression, while upregulated targets of downregulated miRNAs are linked to energy sensing and oxidative metabolism. Furthermore, integration of miRNA and mRNA profiles with proteomes and reporter metabolites revealed that proteins encoded in mRNA targets, and their associated metabolites, mediate fatty acid oxidation and are enriched as the heart develops.This study revealed the small RNAome of the maturing human fetal heart. Furthermore, our findings suggest that coordinated activation and repression of miRNA expression throughout mid-gestation is essential to establish a dynamic miRNA-mRNA-protein network that decreases cardiomyocyte proliferation potential while increasing the oxidative capacity of the maturing human fetal heart.
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Project description:Objectives: The idiopathic inflammatory myopathies (IIMs) are heterogeneous autoimmune conditions of skeletal muscle inflammation and weakness. MicroRNAs (miRNAs) are short, non-coding RNA which regulate gene expression of target mRNAs. The aim of this study was to profile miRNA and mRNA in IIM and identify miRNA-mRNA relationships which may be relevant to disease. Materials and methods: mRNA and miRNA in whole blood samples from 7 polymyositis (PM), 7 dermatomyositis (DM), 5 inclusion body myositis (IBM) and 5 non-myositis controls was profiled using next generation RNA sequencing. Gene ontology and pathway analyses were performed using GOseq and Ingenuity Pathway Analysis. Dysregulation of miRNAs and opposite dysregulation of predicted target mRNAs in IIM subgroups was validated using RTqPCR and investigated by transfecting human skeletal muscle cells with miRNA mimic. Results Analysis of differentially expressed genes showed that interferon signalling and anti-viral response pathways were upregulated in PM and DM compared to controls. An anti-Jo1 autoantibody positive subset of PM and DM (n=5) had more significant upregulation and predicted activation of interferon signalling and highlighted T-helper (Th1 and Th2) cell pathways. In miRNA profiling miR-96-5p was significantly upregulated in PM, DM and the anti-Jo1positive subset. RTqPCR replicated miR-96-5p upregulation and predicted mRNA target (ADK, CD28 and SLC4A10) downregulation. Transfection of a human skeletal muscle cell line with miR-96-5p mimic resulted in significant downregulation of ADK. Conclusion: MiRNA and mRNA profiling identified dysregulation of interferon signalling, anti-viral response and T-helper cell pathways, and indicates a possible role for miR-96-5p regulation of ADK in pathogenesis of IIM.
2019-07-31 | GSE125977 | GEO
Project description:MicroRNA (miRNA) are a class of small non-coding RNAs that act on the stability and the translation efficiency of their mRNA targets. Several evidences suggest that they play a role in tumorigenesis. So far, all types of thyroid tumors have been studied for miRNA expression except autonomous adenomas (AA), benign tumors characterized by the constitutive activation of the cAMP-dependent pathway, leading to a functional hyperactivity of the tissues. The objective of the study was to identify the deregulated miRNA in AA and to correlate the data with mRNA regulation observed in the same samples. AA and their corresponding adjacent tissues were hybridized on miRNA and mRNA microarrays. In order to investigate the correlation between both datasets and to identify mRNA regulations, bioinformatic mRNA target prediction softwares were used. 12 miRNAs were found as downregulated and 1 as upregulated in the tumors. Members of 3 different miR-families (miR-19, miR-29 and miR-135 families) were found among the regulated miRNA. By bioinformatic predictions we searched, among the mRNA microarray data, for regulated mRNA which could be targeted by the modulated miRNA. A great enrichment in mRNA encoding proteins involved in the extracellular matrix organization, as well as different phosphodiesterases were identified among the putative targets. The global miRNA profiles are not greatly modified, confirming the definition of these tumors as minimal deviation tumors. These results support a role for miRNA in ECM regulation and tissue remodelling occurring during tumor development, as well as in the retrocontrol of the activated cAMP pathway.
2012-12-31 | GSE33079 | GEO
Project description:MicroRNA (miRNA) are a class of small non-coding RNAs that act on the stability and the translation efficiency of their mRNA targets. Several evidences suggest that they play a role in tumorigenesis. So far, all types of thyroid tumors have been studied for miRNA expression except autonomous adenomas (AA), benign tumors characterized by the constitutive activation of the cAMP-dependent pathway, leading to a functional hyperactivity of the tissues. The objective of the study was to identify the deregulated miRNA in AA and to correlate the data with mRNA regulation observed in the same samples. AA and their corresponding adjacent tissues were hybridized on miRNA and mRNA microarrays. In order to investigate the correlation between both datasets and to identify mRNA regulations, bioinformatic mRNA target prediction softwares were used. 12 miRNAs were found as downregulated and 1 as upregulated in the tumors. Members of 3 different miR-families (miR-19, miR-29 and miR-135 families) were found among the regulated miRNA. By bioinformatic predictions we searched, among the mRNA microarray data, for regulated mRNA which could be targeted by the modulated miRNA. A great enrichment in mRNA encoding proteins involved in the extracellular matrix organization, as well as different phosphodiesterases were identified among the putative targets. The global miRNA profiles are not greatly modified, confirming the definition of these tumors as minimal deviation tumors. These results support a role for miRNA in ECM regulation and tissue remodelling occurring during tumor development, as well as in the retrocontrol of the activated cAMP pathway. 7 tumors hybridized in dey-swap, compared to thier adjacent normal tissues.
2012-12-31 | E-GEOD-33079 | biostudies-arrayexpress
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2012-01-01 | GSE33703 | GEO
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Project description:Proctor2017 - Identifying microRNA for muscle regeneration during ageing (Mir1_in_muscle)
This model is described in the article:
Using computer simulation
models to investigate the most promising microRNAs to improve
muscle regeneration during ageing
Carole J. Proctor & Katarzyna
Goljanek-Whysall
Nature Scientific Reports
Abstract:
MicroRNAs (miRNAs) regulate gene expression through
interactions with target sites within mRNAs, leading to
enhanced degradation of the mRNA or inhibition of translation.
Skeletal muscle expresses many different miRNAs with important
roles in adulthood myogenesis (regeneration) and myofibre
hypertrophy and atrophy, processes associated with muscle
ageing. However, the large number of miRNAs and their targets
mean that a complex network of pathways exists, making it
difficult to predict the effect of selected miRNAs on
age-related muscle wasting. Computational modelling has the
potential to aid this process as it is possible to combine
models of individual miRNA:target interactions to form an
integrated network. As yet, no models of these interactions in
muscle exist. We created the first model of miRNA:target
interactions in myogenesis based on experimental evidence of
individual miRNAs which were next validated and used to make
testable predictions. Our model confirms that miRNAs regulate
key interactions during myogenesis and can act by promoting the
switch between quiescent/proliferating/differentiating
myoblasts and by maintaining the differentiation process. We
propose that a threshold level of miR-1 acts in the initial
switch to differentiation, with miR-181 keeping the switch on
and miR-378 maintaining the differentiation and miR-143
inhibiting myogenesis.
This model is hosted on
BioModels Database
and identified by:
MODEL1704110000.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2017-09-26 | MODEL1704110000 | BioModels
Project description:Proctor2017 - Identifying microRNA for muscle
regeneration during ageing (Mir181_in_muscle)
This model is described in the article:
Using computer simulation
models to investigate the most promising microRNAs to improve
muscle regeneration during ageing
Carole J. Proctor & Katarzyna
Goljanek-Whysall
Scientific Reports
Abstract:
MicroRNAs (miRNAs) regulate gene expression through
interactions with target sites within mRNAs, leading to
enhanced degradation of the mRNA or inhibition of translation.
Skeletal muscle expresses many different miRNAs with important
roles in adulthood myogenesis (regeneration) and myofibre
hypertrophy and atrophy, processes associated with muscle
ageing. However, the large number of miRNAs and their targets
mean that a complex network of pathways exists, making it
difficult to predict the effect of selected miRNAs on
age-related muscle wasting. Computational modelling has the
potential to aid this process as it is possible to combine
models of individual miRNA:target interactions to form an
integrated network. As yet, no models of these interactions in
muscle exist. We created the first model of miRNA:target
interactions in myogenesis based on experimental evidence of
individual miRNAs which were next validated and used to make
testable predictions. Our model confirms that miRNAs regulate
key interactions during myogenesis and can act by promoting the
switch between quiescent/proliferating/differentiating
myoblasts and by maintaining the differentiation process. We
propose that a threshold level of miR-1 acts in the initial
switch to differentiation, with miR-181 keeping the switch on
and miR-378 maintaining the differentiation and miR-143
inhibiting myogenesis.
This model is hosted on
BioModels Database
and identified by:
MODEL1704110001.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2017-09-26 | MODEL1704110001 | BioModels
Project description:Proctor2017 - Identifying microRNA for muscle
regeneration during ageing (Mir143_in_muscle)
This model is described in the article:
Using computer simulation
models to investigate the most promising microRNAs to improve
muscle regeneration during ageing
Carole J. Proctor & Katarzyna
Goljanek-Whysall
Scientific Reports
Abstract:
MicroRNAs (miRNAs) regulate gene expression through
interactions with target sites within mRNAs, leading to
enhanced degradation of the mRNA or inhibition of translation.
Skeletal muscle expresses many different miRNAs with important
roles in adulthood myogenesis (regeneration) and myofibre
hypertrophy and atrophy, processes associated with muscle
ageing. However, the large number of miRNAs and their targets
mean that a complex network of pathways exists, making it
difficult to predict the effect of selected miRNAs on
age-related muscle wasting. Computational modelling has the
potential to aid this process as it is possible to combine
models of individual miRNA:target interactions to form an
integrated network. As yet, no models of these interactions in
muscle exist. We created the first model of miRNA:target
interactions in myogenesis based on experimental evidence of
individual miRNAs which were next validated and used to make
testable predictions. Our model confirms that miRNAs regulate
key interactions during myogenesis and can act by promoting the
switch between quiescent/proliferating/differentiating
myoblasts and by maintaining the differentiation process. We
propose that a threshold level of miR-1 acts in the initial
switch to differentiation, with miR-181 keeping the switch on
and miR-378 maintaining the differentiation and miR-143
inhibiting myogenesis.
This model is hosted on
BioModels Database
and identified by:
MODEL1704110003.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2017-09-26 | MODEL1704110003 | BioModels