cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.28630858
title: Comprehensive analysis of eccDNA characteristics and associated genes expression in peripheral blood of ASLE and ISLE patients

description: To explore SLE staging markers, we analyzed eccDNA in plasma using circular sequencing, comparing healthy controls (HC), active SLE (ASLE), and inactive SLE (ISLE) patients. We found higher eccDNA levels and lower GC content in ASLE and ISLE compared to healthy controls, with a negative correlation between GC content and anti-daDNA, C3, and C4 levels in SLE and HC samples. Differential expression of exon-derived eccGenes in ASLE and ISLE suggests their role in SLE development, with KEGG analysis showing enrichment in SLE-related pathways for these differentially expressed genes. By protein–protein interactions network analysis we found 9 exon-derived eccGenes that were significantly differentially expressed and scored high in both ISLE-HC and ASLE-ISLE as diagnostic criteria for differentiating different disease stages of SLE. In conclusion, the present study reveals that eccDNA length GC content as well as chromosomal distribution in ASLE, ISLE and HC suggests that with eccDNA is associated with the creation of SLE, suggesting GC count of eccDNA as a diagnostic marker for systemic lupus erythematosus. Significant changes in the abundance of eccDNA-related genes from exons such as SOS1, GAD2, BCL11B, PPT1, and GCNT3 were observed in ISLE as compared to ASLE and HC groups and were significantly correlated with SLEDAI-2K. This suggests that these exon-derived eccGenes may play a role in the development and progression of the disease. Consequently, the abundance levels of these exon-derived eccGenes could potentially assist in distinguishing different stages of SLE, beyond a confirmed diagnosis, thus serving as possible biomarkers for the condition.
DOI: 10.6084/m9.figshare.28630858.v1
title: Comprehensive analysis of eccDNA characteristics and associated genes expression in peripheral blood of ASLE and ISLE patients

description: To explore SLE staging markers, we analyzed eccDNA in plasma using circular sequencing, comparing healthy controls (HC), active SLE (ASLE), and inactive SLE (ISLE) patients. We found higher eccDNA levels and lower GC content in ASLE and ISLE compared to healthy controls, with a negative correlation between GC content and anti-daDNA, C3, and C4 levels in SLE and HC samples. Differential expression of exon-derived eccGenes in ASLE and ISLE suggests their role in SLE development, with KEGG analysis showing enrichment in SLE-related pathways for these differentially expressed genes. By protein–protein interactions network analysis we found 9 exon-derived eccGenes that were significantly differentially expressed and scored high in both ISLE-HC and ASLE-ISLE as diagnostic criteria for differentiating different disease stages of SLE. In conclusion, the present study reveals that eccDNA length GC content as well as chromosomal distribution in ASLE, ISLE and HC suggests that with eccDNA is associated with the creation of SLE, suggesting GC count of eccDNA as a diagnostic marker for systemic lupus erythematosus. Significant changes in the abundance of eccDNA-related genes from exons such as SOS1, GAD2, BCL11B, PPT1, and GCNT3 were observed in ISLE as compared to ASLE and HC groups and were significantly correlated with SLEDAI-2K. This suggests that these exon-derived eccGenes may play a role in the development and progression of the disease. Consequently, the abundance levels of these exon-derived eccGenes could potentially assist in distinguishing different stages of SLE, beyond a confirmed diagnosis, thus serving as possible biomarkers for the condition.
DOI: 10.6084/m9.figshare.29062484
title: LncRNA SCARNA8 promotes atherosclerotic plaque instability by inhibiting macrophage efferocytosis

description: In recent years, findings suggest that long noncoding RNAs (lncRNAs) are closely related to the development of atherosclerosis (AS), but there is a lack of studies on the involvement of lncRNA-regulated cytosolic burial in the regulation of AS. In this study, we investigated the mechanism by which lncRNA SCARNA8 affects macrophage cell burial to regulate AS. The cytosolic burial-associated target gene regulated by lncRNA SCARNA8 was PPARG. LncRNA SCARNA8 was increased in the carotid unstable plaque group, whereas PPARG was decreased. Ox-LDL led to the up-regulation of lncRNA SCARNA8 expression and apoptosis in Raw264.7 cells in a time-, concentration-dependent manner. Knockdown of lncRNA SCARNA8 upregulated PPARG and reduced apoptosis in Raw264.7 cells. In addition, knockdown of lncRNA SCARNA8 improved the stability of atherosclerotic plaques by promoting cellular burial of Raw264.7 cells. LncRNA SCARNA8 is a key regulator of plaque vulnerability, and targeting lncRNA SCARNA8 May provide a novel means for the prevention and treatment of AS.
DOI: 10.6084/m9.figshare.29062484.v1
title: LncRNA SCARNA8 promotes atherosclerotic plaque instability by inhibiting macrophage efferocytosis

description: In recent years, findings suggest that long noncoding RNAs (lncRNAs) are closely related to the development of atherosclerosis (AS), but there is a lack of studies on the involvement of lncRNA-regulated cytosolic burial in the regulation of AS. In this study, we investigated the mechanism by which lncRNA SCARNA8 affects macrophage cell burial to regulate AS. The cytosolic burial-associated target gene regulated by lncRNA SCARNA8 was PPARG. LncRNA SCARNA8 was increased in the carotid unstable plaque group, whereas PPARG was decreased. Ox-LDL led to the up-regulation of lncRNA SCARNA8 expression and apoptosis in Raw264.7 cells in a time-, concentration-dependent manner. Knockdown of lncRNA SCARNA8 upregulated PPARG and reduced apoptosis in Raw264.7 cells. In addition, knockdown of lncRNA SCARNA8 improved the stability of atherosclerotic plaques by promoting cellular burial of Raw264.7 cells. LncRNA SCARNA8 is a key regulator of plaque vulnerability, and targeting lncRNA SCARNA8 May provide a novel means for the prevention and treatment of AS.
DOI: 10.15468/dl.he5akg
title: Occurrence Download

description: A dataset containing 50834 species occurrences available in GBIF matching the query:
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 "TaxonKey is Myctophidae",
 "HasCoordinate is true",
 "Geometry POLYGON((-20.000000 -75.000000, 160.000000 -75.000000, 160.000000 -30.000000, -20.000000 -30.000000, -20.000000 -75.000000))"
 ]
}

 The dataset includes 50834 records from 82 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0045129-251120083545085/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.6084/m9.figshare.29824891
title: Methylation profile of individuals with sickle cell trait

description: Sickle cell trait (SCT) is due to heterozygosity for the β-globin sickle cell mutation. SCT recently has been associated with increased risk of various adverse health outcomes. DNA methylation (DNAm) is one potential mechanism by which SCT may impact disease risk. To identify DNAm sites associated with SCT, we conducted an epigenome-wide association (EWAS) meta-analysis using whole blood Illumina EPIC array data available in a total of 3,677 African American participants (including 1,071 with SCT) from the Women’s Health Initiative and Jackson Heart Study. We identified 103 differentially methylated CpGs and 119 differentially methylated regions associated with SCT. The strongest signals were hypermethylated cis loci within predicted regulatory elements within or near the β-globin gene cluster on chromosome 11. Beyond the globin locus, SCT-associated DMPs were enriched in genes involved in redox regulation and oxidative stress. We also demonstrate an association of SCT with differences in biological age and epigenetic age acceleration, though the pattern and strength of association differ according to the epigenetic clock used. Specifically, more recent epigenetic clocks that incorporate clinical phenotypes or laboratory biomarkers related to adverse health outcomes are associated with accelerated aging among individuals with SCT compared to African American controls. Our results lay the groundwork for future study of the role of DNAm in biologic aging and related health outcomes among individuals with SCT.
DOI: 10.6084/m9.figshare.29824891.v1
title: Methylation profile of individuals with sickle cell trait

description: Sickle cell trait (SCT) is due to heterozygosity for the β-globin sickle cell mutation. SCT recently has been associated with increased risk of various adverse health outcomes. DNA methylation (DNAm) is one potential mechanism by which SCT may impact disease risk. To identify DNAm sites associated with SCT, we conducted an epigenome-wide association (EWAS) meta-analysis using whole blood Illumina EPIC array data available in a total of 3,677 African American participants (including 1,071 with SCT) from the Women’s Health Initiative and Jackson Heart Study. We identified 103 differentially methylated CpGs and 119 differentially methylated regions associated with SCT. The strongest signals were hypermethylated cis loci within predicted regulatory elements within or near the β-globin gene cluster on chromosome 11. Beyond the globin locus, SCT-associated DMPs were enriched in genes involved in redox regulation and oxidative stress. We also demonstrate an association of SCT with differences in biological age and epigenetic age acceleration, though the pattern and strength of association differ according to the epigenetic clock used. Specifically, more recent epigenetic clocks that incorporate clinical phenotypes or laboratory biomarkers related to adverse health outcomes are associated with accelerated aging among individuals with SCT compared to African American controls. Our results lay the groundwork for future study of the role of DNAm in biologic aging and related health outcomes among individuals with SCT.
DOI: 10.15468/dl.dj9fdd
title: Occurrence Download

description: A dataset containing 0 species occurrences available in GBIF matching the query:
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 The dataset includes 0 records from 0 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0045172-251120083545085/datasets/export for details.
DOI: 10.6084/m9.figshare.29134985
title: Epigenetic signatures of maternal-fetal health: insights from cord blood and placenta

description: The placenta is vital for fetal growth, and its methylation patterns reflect placental function, affecting the fetus and providing insights into disease origins. While cord blood methylation is convenient for assessing the fetal environment, methylation profiles vary by tissue due to variance in cell populations, function, and life stage. As tissue differences extensively contribute to the DNA methylation patterns, using surrogate samples such as cord blood may result in inconsistent findings. In this study, we aim to quantify the correlation of <i>cytosine-phosphate-guanine dinucleotides (CpGs) between paired cord blood and placenta</i> samples. Using the Infinium Human Methylation 450 K BeadChip, we compared methylation patterns in cord blood mononuclear cells (CBMC; <i>n</i> = 54), the maternally-facing side of placental tissue (MP; <i>n</i> = 68), and the fetal-facing side of placental tissue (FP; <i>n</i> = 67). Methylation patterns from the FP (6,021 CpGs) were significantly correlated with CBMC compared to the MP (2,862 CpGs). These CpGs were related to the biological (mitotic cell) process and molecular function (ribonucleoprotein complex binding). Our findings quantified CpG site correlation between cord blood and placenta, providing a valuable reference for future studies on placental health that rely on cord blood methylation in the absence of placental biospecimens.
DOI: 10.6084/m9.figshare.29134985.v1
title: Epigenetic signatures of maternal-fetal health: insights from cord blood and placenta

description: The placenta is vital for fetal growth, and its methylation patterns reflect placental function, affecting the fetus and providing insights into disease origins. While cord blood methylation is convenient for assessing the fetal environment, methylation profiles vary by tissue due to variance in cell populations, function, and life stage. As tissue differences extensively contribute to the DNA methylation patterns, using surrogate samples such as cord blood may result in inconsistent findings. In this study, we aim to quantify the correlation of <i>cytosine-phosphate-guanine dinucleotides (CpGs) between paired cord blood and placenta</i> samples. Using the Infinium Human Methylation 450 K BeadChip, we compared methylation patterns in cord blood mononuclear cells (CBMC; <i>n</i> = 54), the maternally-facing side of placental tissue (MP; <i>n</i> = 68), and the fetal-facing side of placental tissue (FP; <i>n</i> = 67). Methylation patterns from the FP (6,021 CpGs) were significantly correlated with CBMC compared to the MP (2,862 CpGs). These CpGs were related to the biological (mitotic cell) process and molecular function (ribonucleoprotein complex binding). Our findings quantified CpG site correlation between cord blood and placenta, providing a valuable reference for future studies on placental health that rely on cord blood methylation in the absence of placental biospecimens.
DOI: 10.6084/m9.figshare.29413831
title: <i>PIK3R1</i> and <i>G0S2</i> are human placenta-specific imprinted genes associated with germline-inherited maternal DNA methylation

description: Genomic imprinting is the parent-of-origin specific monoallelic expression of genes that result from complex epigenetic interactions. It is often achieved by monoallelic 5-methylcytosine, resulting in the formation of differentially methylated regions (DMRs). These show a bias towards oocyte-derived methylation and survive reprogramming in the pre-implantation embryo. Imprinting is widespread in the human placenta. We have recently performed whole-genome screens for novel imprinted placenta-specific germline DMRs (gDMRs) by comparing methylomes of gametes, blastocysts and various somatic tissues, including placenta. We observe that, unlike conventional imprinting, for which methylation at gDMRs is observed in all tissues, placenta-specific imprinting is associated with transient gDMRs, present only in the pre-implantation embryo and extra-embryonic lineages. To expand the list of <i>bona fide</i> imprinted genes subject to placenta-specific imprinting, we reinvestigated our list of candidate loci and characterized two novel imprinted genes, <i>PIK3R1</i> and <i>G0S2</i>, both of which display polymorphic imprinting. Interrogation of placenta single-cell RNA-seq datasets, as well as cell-type methylation profiles, revealed complex cell-type specificity. We further interrogated their methylation and expression in placental samples from complicated pregnancies, but failed to identify differences between intrauterine growth restricted or pre-eclamptic samples and controls, suggesting they are not involved in these conditions. The promoter of <i>G0S2</i> overlaps an oocyte-derived placenta-specific gDMR.The promoter of <i>PIK3R1</i> isoform 3 is embedded within an oocyte-derived placenta-specific gDMR.Allelic methylation at the <i>PIK3R1</i> isoform 3 is restricted to trophoblast.The orthologues <i>Pik3r1</i> and <i>G0s2</i> are not imprinted in the mouse placenta. The promoter of <i>G0S2</i> overlaps an oocyte-derived placenta-specific gDMR. The promoter of <i>PIK3R1</i> isoform 3 is embedded within an oocyte-derived placenta-specific gDMR. Allelic methylation at the <i>PIK3R1</i> isoform 3 is restricted to trophoblast. The orthologues <i>Pik3r1</i> and <i>G0s2</i> are not imprinted in the mouse placenta.
DOI: 10.6084/m9.figshare.29413831.v1
title: <i>PIK3R1</i> and <i>G0S2</i> are human placenta-specific imprinted genes associated with germline-inherited maternal DNA methylation

description: Genomic imprinting is the parent-of-origin specific monoallelic expression of genes that result from complex epigenetic interactions. It is often achieved by monoallelic 5-methylcytosine, resulting in the formation of differentially methylated regions (DMRs). These show a bias towards oocyte-derived methylation and survive reprogramming in the pre-implantation embryo. Imprinting is widespread in the human placenta. We have recently performed whole-genome screens for novel imprinted placenta-specific germline DMRs (gDMRs) by comparing methylomes of gametes, blastocysts and various somatic tissues, including placenta. We observe that, unlike conventional imprinting, for which methylation at gDMRs is observed in all tissues, placenta-specific imprinting is associated with transient gDMRs, present only in the pre-implantation embryo and extra-embryonic lineages. To expand the list of <i>bona fide</i> imprinted genes subject to placenta-specific imprinting, we reinvestigated our list of candidate loci and characterized two novel imprinted genes, <i>PIK3R1</i> and <i>G0S2</i>, both of which display polymorphic imprinting. Interrogation of placenta single-cell RNA-seq datasets, as well as cell-type methylation profiles, revealed complex cell-type specificity. We further interrogated their methylation and expression in placental samples from complicated pregnancies, but failed to identify differences between intrauterine growth restricted or pre-eclamptic samples and controls, suggesting they are not involved in these conditions. The promoter of <i>G0S2</i> overlaps an oocyte-derived placenta-specific gDMR.The promoter of <i>PIK3R1</i> isoform 3 is embedded within an oocyte-derived placenta-specific gDMR.Allelic methylation at the <i>PIK3R1</i> isoform 3 is restricted to trophoblast.The orthologues <i>Pik3r1</i> and <i>G0s2</i> are not imprinted in the mouse placenta. The promoter of <i>G0S2</i> overlaps an oocyte-derived placenta-specific gDMR. The promoter of <i>PIK3R1</i> isoform 3 is embedded within an oocyte-derived placenta-specific gDMR. Allelic methylation at the <i>PIK3R1</i> isoform 3 is restricted to trophoblast. The orthologues <i>Pik3r1</i> and <i>G0s2</i> are not imprinted in the mouse placenta.
DOI: 10.6084/m9.figshare.29413831.v2
title: <i>PIK3R1</i> and <i>G0S2</i> are human placenta-specific imprinted genes associated with germline-inherited maternal DNA methylation

description: Genomic imprinting is the parent-of-origin specific monoallelic expression of genes that result from complex epigenetic interactions. It is often achieved by monoallelic 5-methylcytosine, resulting in the formation of differentially methylated regions (DMRs). These show a bias towards oocyte-derived methylation and survive reprogramming in the pre-implantation embryo. Imprinting is widespread in the human placenta. We have recently performed whole-genome screens for novel imprinted placenta-specific germline DMRs (gDMRs) by comparing methylomes of gametes, blastocysts and various somatic tissues, including placenta. We observe that, unlike conventional imprinting, for which methylation at gDMRs is observed in all tissues, placenta-specific imprinting is associated with transient gDMRs, present only in the pre-implantation embryo and extra-embryonic lineages. To expand the list of <i>bona fide</i> imprinted genes subject to placenta-specific imprinting, we reinvestigated our list of candidate loci and characterized two novel imprinted genes, <i>PIK3R1</i> and <i>G0S2</i>, both of which display polymorphic imprinting. Interrogation of placenta single-cell RNA-seq datasets, as well as cell-type methylation profiles, revealed complex cell-type specificity. We further interrogated their methylation and expression in placental samples from complicated pregnancies, but failed to identify differences between intrauterine growth restricted or pre-eclamptic samples and controls, suggesting they are not involved in these conditions. The promoter of <i>G0S2</i> overlaps an oocyte-derived placenta-specific gDMR.The promoter of <i>PIK3R1</i> isoform 3 is embedded within an oocyte-derived placenta-specific gDMR.Allelic methylation at the <i>PIK3R1</i> isoform 3 is restricted to trophoblast.The orthologues <i>Pik3r1</i> and <i>G0s2</i> are not imprinted in the mouse placenta. The promoter of <i>G0S2</i> overlaps an oocyte-derived placenta-specific gDMR. The promoter of <i>PIK3R1</i> isoform 3 is embedded within an oocyte-derived placenta-specific gDMR. Allelic methylation at the <i>PIK3R1</i> isoform 3 is restricted to trophoblast. The orthologues <i>Pik3r1</i> and <i>G0s2</i> are not imprinted in the mouse placenta.
DOI: 10.6084/m9.figshare.29291251
title: The myoblast methylome: multiple types of associations with chromatin and transcription

description: Epigenetic changes are implicated in development, repair, and physiology of postnatal skeletal muscle (SkM). We generated methylomes for human myoblasts (SkM progenitor cells) and determined myoblast differentially methylated regions (DMRs) for comparison to the epigenomics and transcriptomics of diverse cell types. Analyses were from global genomic and single-gene perspectives and included reporter gene assays. One atypical finding was the association of promoter-adjacent hypermethylation in myoblasts with transcription turn-on, but at downmodulated levels, for certain genes (<i>e.g</i>., <i>SIM2</i> and <i>TWIST1</i>). In contrast, brain-specific <i>OLIG2</i> was in repressed chromatin and silent in most cell types but linked to hypermethylated DMRs specifically in myoblasts. The <i>OLIG2</i>-linked DMRs might be needed because of the overlapping or nearby binding of myogenic differentiation protein 1 (MYOD). We found genome-wide overlap of DMRs with MYOD or CCCTC-binding factor (CTCF) binding sites in myoblasts that is consistent with the importance of MYOD, as well as CTCF, in organizing myoblast transcription-enhancing chromatin interactions. We also observed some gene upregulation correlated with a special association of regional DNA hypomethylation with H3K36me3, H3K27ac, and H3K4me1 enrichment. Our study highlights unusual relationships between epigenetics and gene expression that illustrate the interplay between DNA methylation and chromatin epigenetics in the regulation of transcription.