Small RNA reads sperm parental obesity
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB33337 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Obesity is a global rising problem with epidemiological dimension. Obese parents can have programming effects on their offspring leading to obesity and associated diseases in later life. This constitutes a vicious circle. Epidemiological data and studies in rodents demonstrated differential programming effects in male and female offspring, but the timing of their developmental origin is not known. This study investigated if sex-specific programming effects of parental obesity can already be detected in the pre-implantation period. Diet induced obese male or female mice were mated with normal-weight partners and blastocysts were recovered. Gene expression profiling revealed sex-specific responses of the blastocyst transcriptome to maternal and paternal obesity. The changes in the transcriptome of male blastocysts were more pronounced than those of female blastocysts, with a stronger impact of paternal than of maternal obesity. The sperm of obese mice revealed an increased abundance of several miRNAs compared to lean mice. Our study indicates that sex-specific programming effects of parental obesity already start in the pre‑implantation period and reveals specific alterations of the sperm miRNA profile as mechanistic link to programming effects of paternal obesity.
2019-07-07 | GSE133915 | GEO
Project description:Obesity is a global rising problem with epidemiological dimension. Obese parents can have programming effects on their offspring leading to obesity and associated diseases in later life. This constitutes a vicious circle. Epidemiological data and studies in rodents demonstrated differential programming effects in male and female offspring, but the timing of their developmental origin is not known. This study investigated if sex-specific programming effects of parental obesity can already be detected in the pre-implantation period. Diet induced obese male or female mice were mated with normal-weight partners and blastocysts were recovered. Gene expression profiling revealed sex-specific responses of the blastocyst transcriptome to maternal and paternal obesity. The changes in the transcriptome of male blastocysts were more pronounced than those of female blastocysts, with a stronger impact of paternal than of maternal obesity. The sperm of obese mice revealed an increased abundance of several miRNAs compared to lean mice. Our study indicates that sex-specific programming effects of parental obesity already start in the pre‑implantation period and reveals specific alterations of the sperm miRNA profile as mechanistic link to programming effects of paternal obesity.
2019-07-07 | GSE133914 | GEO
Project description:Obesity is a global rising problem with epidemiological dimension. Obese parents can have programming effects on their offspring leading to obesity and associated diseases in later life. This constitutes a vicious circle. Epidemiological data and studies in rodents demonstrated differential programming effects in male and female offspring, but the timing of their developmental origin is not known. This study investigated if sex-specific programming effects of parental obesity can already be detected in the pre-implantation period. Diet induced obese male or female mice were mated with normal-weight partners and blastocysts were recovered. Gene expression profiling revealed sex-specific responses of the blastocyst transcriptome to maternal and paternal obesity. The changes in the transcriptome of male blastocysts were more pronounced than those of female blastocysts, with a stronger impact of paternal than of maternal obesity. The sperm of obese mice revealed an increased abundance of several miRNAs compared to lean mice. Our study indicates that sex-specific programming effects of parental obesity already start in the pre‑implantation period and reveals specific alterations of the sperm miRNA profile as mechanistic link to programming effects of paternal obesity. We used microarrays to analyze the transcriptomes of sex-sorted blastocysts of mice, with one parent (either mother or father) being obese at the time of conception and compared it to the transcriptome of blasocysts of peri-conceptionally lean parents.
2019-07-04 | GSE133767 | GEO
Project description:Sex-specific programming effects of parental obesity in pre-implantation embryonic development [RNASeq Data of Sperm]
| PRJNA553001 | ENA
Project description:Sex-specific programming effects of parental obesity in pre-implantation embryonic development
| PRJNA553000 | ENA
Project description:Sex-specific programming effects of parental obesity in pre-implantation embryonic development [RNASeq Data of Oocytes]
| PRJNA553002 | ENA
Project description:Sex-specific programming effects of parental obesity in pre-implantation embryonic development_Microarray data on blastocyst transcriptomes
| PRJNA552488 | ENA
Project description:Growing evidence point towards a strong contribution of paternal factors in placental health with implications in adult-onset complex disease risk. We have recently demonstrated that paternal diet-induced obesity alters sperm histone methylation and is associated with metabolic disturbances in the next generation. Diet-sensitive epigenetic regions in sperm were found at genes involved in trophectoderm and placental development, and corresponded to epigenetic and gene expression profiles in these tissues. We sought to investigate whether paternal diet-induced obesity before conception can alter the placental transcriptome, and whether differential gene expression corresponds with sperm obesity-associated epigenetic signatures. C57BL6/J males were fed either a control or high-fat diet for 10 weeks beginning at 6 weeks of age. They were then bred to control-fed C57BL6/J females to induce pregnancies and E14.5 placentas were collected. RNA-sequencing was performed (n=4 per group per sex) to detect sex-specific transcriptional changes associated with paternal diet. At necropsy, sperm was collected for chromatin immunoprecipitation followed by sequencing (ChIP-seq; n=3 per group) targeting histone H3 lysine 4 tri-methylation (H3K4me3) to detect obesity-induced changes in H3K4me3 enrichment. There were sex-specific differentially expressed genes in placentas with some overlapping with promoters showing obesity-associated sperm epimutations. A deconvolution analysis using single-cell RNA-seq data from mouse E14.5 placenta (Han et al., Cell, 2018) revealed significant differences in trophoblast subtype proportions in placentas derived from HFD sires. This study highlights a previously underappreciated role of the placenta at the origin of paternally-induced metabolic disturbances in offspring.
2022-09-09 | GSE207313 | GEO
Project description:Growing evidence point towards a strong contribution of paternal factors in placental health with implications in adult-onset complex disease risk. We have recently demonstrated that paternal diet-induced obesity alters sperm histone methylation and is associated with metabolic disturbances in the next generation. Diet-sensitive epigenetic regions in sperm were found at genes involved in trophectoderm and placental development, and corresponded to epigenetic and gene expression profiles in these tissues. We sought to investigate whether paternal diet-induced obesity before conception can alter the placental transcriptome, and whether differential gene expression corresponds with sperm obesity-associated epigenetic signatures. C57BL6/J males were fed either a control or high-fat diet for 10 weeks beginning at 6 weeks of age. They were then bred to control-fed C57BL6/J females to induce pregnancies and E14.5 placentas were collected. RNA-sequencing was performed (n=4 per group per sex) to detect sex-specific transcriptional changes associated with paternal diet. At necropsy, sperm was collected for chromatin immunoprecipitation followed by sequencing (ChIP-seq; n=3 per group) targeting histone H3 lysine 4 tri-methylation (H3K4me3) to detect obesity-induced changes in H3K4me3 enrichment. There were sex-specific differentially expressed genes in placentas with some overlapping with promoters showing obesity-associated sperm epimutations. A deconvolution analysis using single-cell RNA-seq data from mouse E14.5 placenta (Han et al., Cell, 2018) revealed significant differences in trophoblast subtype proportions in placentas derived from HFD sires. This study highlights a previously underappreciated role of the placenta at the origin of paternally-induced metabolic disturbances in offspring.
2022-09-09 | GSE207325 | GEO
Project description:While obesity has links to poor semen parameters and reduced fertility, the causative links between obesity and male infertility are unclear, particularly on a molecular level. We investigated how obesity impacts the human sperm proteome, to further understand any implications for fertility. Sperm protein lysates from 5 healthy weight (BMI < 25) or obese (BMI>30) men were FASP digested, analysed by LC-MS/MS and quantitatively compared by label free quantification. Findings were confirmed for representative proteins by immunofluorescence staining. 2034 proteins were confidently identified, with 24 significantly less abundant (fold change <0.5) and 3 significantly more abundant (fold change >1.5)in sperm of obese men. These proteins were involved in a range of biological processes, including oxidative stress (GSS, NDUFS2, JAGN1, USP14, ADH5), inflammation (SUGT1, LTA4H), translation (EIF3F, EIF4A2, CSNK1G1), DNA damage repair (UBEA4) and sperm function (NAPA, RNPEP, BANF2). These results suggest that oxidative stress and inflammation are closely tied to reproductive dysfunction in obese men. These processes likely impact protein translation and folding during spermatogenesis, leading to poor sperm function and subfertility. The observation of these changes in normozoospermic men further suggests that traditional clinical semen assessment fails to detect important biological changes in spermatozoa which may compromise fertility.
2020-02-18 | PXD014849 | Pride