Age and poverty status alter the coding and noncoding transcriptome
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PROVIDER: PRJNA508945 | ENA |
REPOSITORIES: ENA
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Project description:Emerging evidence indicates that noncoding RNAs play important regulatory roles during aging and the development of chronic disease. The functional roles of long noncoding RNAs (lncRNAs) in physiology and disease are under intense examination. However, little is known about lncRNAs in the context of human aging and socio-environmental conditions. Microarray profiling of lncRNAs and mRNAs in young and old white and African American (AA) males living above or below poverty revealed robust changes in both lncRNAs and mRNAs with age and poverty status in white males, but not in AA males. We validated the changes in lncRNAs in an expanded cohort; CDT-3247F14.2, GAS5, H19, TERC and MEG3 changed significantly with age, whereas AK022914, GAS5, KB-1047C11.2, MEG3 and XLOC_003262 changed significantly with poverty. Pathway analysis revealed that mitochondrial function and response to DNA damage and stress were enriched in younger individuals. Pathways of response to stress, viral infection, and immune signals were enriched in individuals living above poverty. These data show that both human age and a marker of social adversity influence lncRNA expression patterns. These data may provide insight into the molecular pathways underlying aging and social factors that affect disparities in aging and disease.
2019-03-19 | GSE123497 | GEO
Project description:Emerging evidence indicates that noncoding RNAs play important regulatory roles during aging and the development of chronic disease. The functional roles of long noncoding RNAs (lncRNAs) in physiology and disease are under intense examination. However, little is known about lncRNAs in the context of human aging and socio-environmental conditions. Microarray profiling of lncRNAs and mRNAs in young and old white and African American (AA) males living above or below poverty revealed robust changes in both lncRNAs and mRNAs with age and poverty status in white males, but not in AA males. We validated the changes in lncRNAs in an expanded cohort; CDT-3247F14.2, GAS5, H19, TERC and MEG3 changed significantly with age, whereas AK022914, GAS5, KB-1047C11.2, MEG3 and XLOC_003262 changed significantly with poverty. Pathway analysis revealed that mitochondrial function and response to DNA damage and stress were enriched in younger individuals. Pathways of response to stress, viral infection, and immune signals were enriched in individuals living above poverty. These data show that both human age and a marker of social adversity influence lncRNA expression patterns. These data may provide insight into the molecular pathways underlying aging and social factors that affect disparities in aging and disease.
2019-03-19 | GSE123499 | GEO
Project description:Age and poverty status alter the coding and noncoding transcriptome [White]
| PRJNA508948 | ENA
Project description:Age and poverty status alter the coding and noncoding transcriptome [African American]
| PRJNA508950 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2019-03-19 | GSE123500 | GEO
Project description:Emerging evidence indicates that noncoding RNAs play regulatory roles in aging and disease. The functional roles of long noncoding RNAs (lncRNAs) in physiology and disease are not completely understood. Little is known about lncRNAs in the context of human aging and socio-environmental conditions. Microarray profiling of lncRNAs and mRNAs from peripheral blood mononuclear cells from young and old white (n=16) and African American (AA) males (n=16) living above or below poverty from the Healthy Aging in Neighborhoods of Diversity across the Life Span study revealed changes in both lncRNAs and mRNAs with age and poverty status in white males, but not in AA males. We validated lncRNA changes in an expanded cohort (n=40); CTD-3247F14.2, GAS5, H19, TERC and MEG3 changed significantly with age, whereas AK022914, GAS5, KB-1047C11.2, MEG3 and XLOC_003262 changed with poverty. Mitochondrial function and response to DNA damage and stress were pathways enriched in younger individuals. Response to stress, viral infection, and immune signals were pathways enriched in individuals living above poverty. These data show that both human age and a marker of social adversity influence lncRNA expression, which may provide insight about molecular pathways underlying aging and social factors that affect disparities in aging and disease.
| S-EPMC6402526 | biostudies-literature
Project description:Socioeconomic status (SES), living in poverty, and other social determinants of health contribute to health disparities in the United States. African American (AA) men living below poverty in Baltimore City have a higher incidence of mortality when compared to either white males or AA females living below poverty. Previous studies in our laboratory and elsewhere suggest that environmental conditions are associated with differential gene expression (DGE) patterns in white blood cells, and this may contribute to the onset of diseases in the immune or cardiovascular systems. DGE have also been associated with hypertension and cardiovascular disease (CVD) and correlate with race and gender. However, no studies have investigated how poverty status associates with DGE between male and female AAs and whites living in Baltimore City. We examined DGE in 52 AA and white participants of the Healthy Aging in Neighborhoods of Diversity across the Life Span (HANDLS) cohort, who were living above or below 125% of the 2004 federal poverty line at time of sample collection. We performed a microarray to assess DGE patterns in peripheral blood mononuclear cells (PBMCs) from these participants. AA males and females living in poverty had the most genes differentially-expressed compared with above poverty controls. Gene ontology (GO) analysis identified unique and overlapping pathways related to the endosome, single-stranded RNA binding, long-chain fatty-acyl-CoA biosynthesis, toll-like receptor signaling, and others within AA males and females living in poverty and compared with their above poverty controls. We performed RT-qPCR to validate top differentially-expressed genes in AA males. We found that KLF6, DUSP2, RBM34, and CD19 are expressed at significantly lower levels in AA males in poverty and KCTD12 is higher compared to above poverty controls. This study serves as initial link to better understand the biological mechanisms of poverty status with health outcomes and disparities.
2020-10-02 | GSE149256 | GEO
Project description:1. Evaluate the diagnostic value of long noncoding RNA (CCAT1) expression by RT-PCR in peripheral blood in colorectal cancer patients versus normal healthy control personal.
2. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in diagnosis of colorectal cancer patients & its relation to tumor staging.
3. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in precancerous colorectal diseases.
4. Compare long noncoding RNA (CCAT1) expression with traditional marker; carcinoembryonic antigen (CEA) and Carbohydrate antigen 19-9 (CA19-9) in diagnosis of colorectal cancer.
| 2330122 | ecrin-mdr-crc
Project description:In marmoset T cells transformed by Herpesvirus saimiri (HVS), a viral U-rich noncoding RNA, HSUR 1, specifically mediates degradation of host microRNA-27 (miR-27). High-throughput sequencing of RNA after crosslinking immunoprecipitation (HITS-CLIP) identified mRNAs targeted by miR-27 as enriched in the T-cell receptor (TCR) signaling pathway, including GRB2. Accordingly, transfection of miR-27 into human T cells attenuates TCR-induced activation of mitogen-activated protein kinases (MAPKs) and induction of CD69. MiR-27 also robustly regulates SEMA7A and IFN-γ, key modulators and effectors of T-cell function. Knockdown or ectopic expression of HSUR 1 alters levels of these proteins in virally-transformed cells. Two other T-lymphotropic γ-herpesviruses, AlHV-1 and OvHV-2, do not produce a noncoding RNA to downregulate miR-27, but instead encode homologs of miR-27 target genes. Thus, oncogenic γ-herpesviruses have evolved diverse strategies to converge on common targets in host T cells. HVS-transformed marmoset T cells were transfected with ASOs against HSUR 1 or control, or with LNAs against miR-27 or control, in replicates; poly A+ RNAs were selected and sequenced on HiSeq 2000.
2014-09-01 | E-GEOD-55185 | biostudies-arrayexpress
Project description:In marmoset T cells transformed by Herpesvirus saimiri (HVS), a viral U-rich noncoding RNA, HSUR 1, specifically mediates degradation of host microRNA-27 (miR-27). High-throughput sequencing of RNA after crosslinking immunoprecipitation (HITS-CLIP) identified mRNAs targeted by miR-27 as enriched in the T-cell receptor (TCR) signaling pathway, including GRB2. Accordingly, transfection of miR-27 into human T cells attenuates TCR-induced activation of mitogen-activated protein kinases (MAPKs) and induction of CD69. MiR-27 also robustly regulates SEMA7A and IFN-γ, key modulators and effectors of T-cell function. Knockdown or ectopic expression of HSUR 1 alters levels of these proteins in virally-transformed cells. Two other T-lymphotropic γ-herpesviruses, AlHV-1 and OvHV-2, do not produce a noncoding RNA to downregulate miR-27, but instead encode homologs of miR-27 target genes. Thus, oncogenic γ-herpesviruses have evolved diverse strategies to converge on common targets in host T cells.
2014-09-01 | GSE55185 | GEO