A global view of the transcriptional profiling of adipose tissue in Chinese Qinchuan cattle using RNA sequencing
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ABSTRACT:
ORGANISM(S): Bos taurus
PROVIDER: GSE47653 | GEO | 2016/06/05
SECONDARY ACCESSION(S): PRJNA207067
REPOSITORIES: GEO
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Project description:Sex condition has been demonstrated to alter meat quality and sex is a major factor that affects the fatty acid composition of lipids of carcass dissectible or intramuscular depot fats. But the possible genetic molecular mechanism of gender causing meat quality differences is not well defined. Qinchuan cattle, Qinghai yak and Guangxi buffalo are three typical indigenous species of cattle in China. Obivious differences of meat quality exist among the three species of cattle. Few studies have been conducted to elucidate the muscle tissue expression of genes involved in pathways and mechanisms leading to meat quality differences beyond the phenotype properties of beef. Bovine Genome Arrays were used to construct muscle expression profiles of the longuissimus dorsi from Qinchuan cattle at 36 months and screen differentially expressed genes in the longuissimus dorsi muscle tissues among different genders of Qinchuan cattle, between Qinchuan cattle and Qinghai yak, and between Qinchuan cattle and Guangxi buffalo.
2009-12-23 | GSE19586 | GEO
Project description:High throughput circRNA sequencing for adipose tissue of Qinchuan cattle
| PRJNA552355 | ENA
Project description:*Background: Adipocytes mainly function as energy storage and endocrine cells. The amount and distribution of fat are important factor that influence the meat quality in the beef industry. Fat depot can be found around internal organ (ometal), beneath the skin (subcutaneous), and between muscles (intramuscular). Different adipose depot showed the biological and genetic difference depending on their location. This inter-depot variation might be influenced by the inherent genetic programing for development of adipose depots. In this study, we used RNA-seq data to investigate the difference in transcriptome of various adipose depots in Hanwoo. *Results: Using RNA-seq, we identified 5797, 2156, and 5455 DEGs in the comparison between OI, OS, and IS respectively (FDR<0.01) and found 853, 48, and 979 DEGs specific to subcutaneous, intramuscular and omental fat respectively. DEGs in intramuscular fat were highly enriched the metabolism related pathways compared to other fat depots. DEGs specific to the omental fat is significantly enriched in PPAR signaling pathway and cell-junction related pathway. In subcutaneous fat, cytokine-cytokine receptor interaction with chemokines (CXC and CC subfamily) was the most significantly enriched the pathways. Interestingly, melanogenesis pathway was associated with the subcutaneous depot. Even though the adipose tissues shared the same pathways for adipocyte differentiation, the regulation of genes were different based on the depot. *Conclusions: We comparatively analyzed the transcripome profile from different adipose tissues using NGS and identified DEGs between adipose depot and specific to depot in Hanwoo animals. The functional annotation analysis of DEGs found that transcriptome profile difference in various adipose tissue of intramuscular, subcutaneous, and ometal fat. whole mRNA sequencing profiles of nine Korean native cattle (nine profiles of omental fat tissue, nine profiles of intramuscular fat tissue, nine profiles of subcutaneous fat tissue and eight profiles of muscle tissue)
2013-07-25 | E-GEOD-39618 | biostudies-arrayexpress
Project description:GeneSeek HD Bovine 77k Genotyping array is used to estimate population structure and ancestry of bovine and evaluate loci responsible for complex traits. Further, copy number variation of bovine can be estimated by GeneSeek HD Bovine 77k Genotyping array. Here, we estimate population structure and ancestry of Qinchuan cattle.
2017-06-15 | GSE100038 | GEO
Project description:Background: Obesity is associated with infiltration of macrophages into adipose tissue. Adipose macrophages may contribute to an elevated inflammatory status by secreting a variety of pro-inflammatory mediators, including TNFalpha and IL-6. Recent data suggest that during diet-induced obesity the phenotype of adipose-resident macrophages changes from alternatively activated macrophages towards a more classical and pro-inflammatory phenotype. Here, we explore the effect of PPARγ-activation on obesity-induced inflammation in 129SV mice fed a high fat diet for 20 weeks. High fat feeding increased bodyweight gain, adipose tissue mass and liver triglycerides. Rosiglitazone treatment further increased adipose mass, reduced liver triglycerides and changed adipose tissue morphology towards smaller adipocytes. Surprisingly, rosiglitazone markedly increased the number of macrophages in adipose tissue, as shown by immunohistochemical analysis and quantification of macrophage marker genes CD68 and F4/80+. In adipose tissue, markers for classically activated macrophages including IL-18 were down regulated whereas markers characteristic for alternatively activated macrophages (Arginase 1, IL-10) were up regulated by rosiglitazone. Importantly, conditioned media from rosiglitazone-treated alternatively activated macrophages neutralized the inhibitory effect of macrophages on 3T3-L1 adipocyte differentiation, suggesting that alternatively activated macrophages may be involved in mediating the effects of rosiglitazone on adipose tissue morphology and mass. Our results suggest that short term rosiglitazone treatment increases infiltration of alternatively activated macrophages in adipose tissue. The alternatively activated macrophages might play a role in PPARγ-dependent expansion and remodeling of adipose tissue. Keywords: metabolic state analysis
2008-04-29 | GSE11295 | GEO
Project description:*Background: Adipocytes mainly function as energy storage and endocrine cells. The amount and distribution of fat are important factor that influence the meat quality in the beef industry. Fat depot can be found around internal organ (ometal), beneath the skin (subcutaneous), and between muscles (intramuscular). Different adipose depot showed the biological and genetic difference depending on their location. This inter-depot variation might be influenced by the inherent genetic programing for development of adipose depots. In this study, we used RNA-seq data to investigate the difference in transcriptome of various adipose depots in Hanwoo. *Results: Using RNA-seq, we identified 5797, 2156, and 5455 DEGs in the comparison between OI, OS, and IS respectively (FDR<0.01) and found 853, 48, and 979 DEGs specific to subcutaneous, intramuscular and omental fat respectively. DEGs in intramuscular fat were highly enriched the metabolism related pathways compared to other fat depots. DEGs specific to the omental fat is significantly enriched in PPAR signaling pathway and cell-junction related pathway. In subcutaneous fat, cytokine-cytokine receptor interaction with chemokines (CXC and CC subfamily) was the most significantly enriched the pathways. Interestingly, melanogenesis pathway was associated with the subcutaneous depot. Even though the adipose tissues shared the same pathways for adipocyte differentiation, the regulation of genes were different based on the depot. *Conclusions: We comparatively analyzed the transcripome profile from different adipose tissues using NGS and identified DEGs between adipose depot and specific to depot in Hanwoo animals. The functional annotation analysis of DEGs found that transcriptome profile difference in various adipose tissue of intramuscular, subcutaneous, and ometal fat.
2013-07-25 | GSE39618 | GEO
Project description:We report the application of the second-generation sequencing technology for microRNA and mRNA gene expression profiling of intramuscular fat (IMF) in castrated male (CM) and intact male 24 months old Qinchuan cattle (IM) to explore the regulation of intramuscular fat deposition. By comparing the mRNA expression profiles of IMF between CM and IM, 580 upregulated and 1120 downregulated genes were identified as differentially expressed genes correlated with castration. The upregulated genes were mainly associated with lipid metabolism, lipogenesis and fatty acid transportation signaling pathway, and the downregulated genes were correlated with immune response, intracellular signal transduction. Concurrently, the DE miRNAs, which are the important player in adipose tissue accumulation induced by castration, were also examined in IMF tissues, and 52 DE miRNAs were identified. Additionally, the expression profiles of selected genes and miRNAs were confirmed by using quantitative real-time PCR (qRT-PCR) assays. Furthermore, by means of integrated analysis, a total of 951 differentially expressed miRNA-Mrna pairs including 103 DE miRNAs and 535 DE mRNAs were found to show a negative correlation and a pair bovine known microRNA-target network was constructed which were supported by targets validation using dual luciferase reporter system. Moreover, the Ingenuity Pathway Analysis (IPA) software was used to construct a molecular interaction network which might involve in regulating IMF after castration. This molecular network is closely associated with lipid metabolism and adipocyte differentiation, which is supported by the functional identification results of bta-let-7i on bovine preadipocytes. These results provided valuable insights into the molecular mechanisms resulting in the IMF phenotype difference between CM and IM cattle.
2018-02-13 | GSE75063 | GEO
Project description:Background: Obesity is associated with infiltration of macrophages into adipose tissue. Adipose macrophages may contribute to an elevated inflammatory status by secreting a variety of pro-inflammatory mediators, including TNFalpha and IL-6. Recent data suggest that during diet-induced obesity the phenotype of adipose-resident macrophages changes from alternatively activated macrophages towards a more classical and pro-inflammatory phenotype. Here, we explore the effect of PPARγ-activation on obesity-induced inflammation in 129SV mice fed a high fat diet for 20 weeks. High fat feeding increased bodyweight gain, adipose tissue mass and liver triglycerides. Rosiglitazone treatment further increased adipose mass, reduced liver triglycerides and changed adipose tissue morphology towards smaller adipocytes. Surprisingly, rosiglitazone markedly increased the number of macrophages in adipose tissue, as shown by immunohistochemical analysis and quantification of macrophage marker genes CD68 and F4/80+. In adipose tissue, markers for classically activated macrophages including IL-18 were down regulated whereas markers characteristic for alternatively activated macrophages (Arginase 1, IL-10) were up regulated by rosiglitazone. Importantly, conditioned media from rosiglitazone-treated alternatively activated macrophages neutralized the inhibitory effect of macrophages on 3T3-L1 adipocyte differentiation, suggesting that alternatively activated macrophages may be involved in mediating the effects of rosiglitazone on adipose tissue morphology and mass. Our results suggest that short term rosiglitazone treatment increases infiltration of alternatively activated macrophages in adipose tissue. The alternatively activated macrophages might play a role in PPARγ-dependent expansion and remodeling of adipose tissue. Keywords: metabolic state analysis Pure bred wild-type (129S1/SvImJ) male mice received a low fat diet or high fat diet for 21 weeks, providing 10 or 45% energy percent in the form of triglycerides (D12450B or D12451, Research Diets, New Brunswick, USA). The lard component in these diets was replaced by palm oil. In the last week of diet intervention, half of the mice receiving the HFD were switched to HFD supplemented with Rosiglitazone (0.01 % wt/wt). Animals were sacrificed in the fed state. Epididymal adipose tissue was excised and frozen in liquid nitrogen. Pooled RNA samples from 5 mice per experimental group were used for microarray analysis. Samples were hybridized on Affymetrix GeneChip Mouse Genome 430-2.0 plus arrays. Five microgram total RNA was labelled according to the Affymetrix One-cycle Target Labeling Assay, fragmented and hybridized according to Affymetrix's protocols.
2008-04-29 | E-GEOD-11295 | biostudies-arrayexpress
Project description:<p>The Finland-United States Investigation of NIDDM Genetics (FUSION) study is a long-term effort to identify genetic variants that predispose to type 2 diabetes (T2D) or that impact the variability of T2D-related quantitative traits (QTs). Skeletal muscle and adipose are major insulin target tissues and play key roles in insulin resistance. We hypothesize that a subset of T2D and related QT variants alter gene expression in skeletal muscle and adipose tissue. For this FUSION Tissue Biopsy Study, we have obtained and are analyzing RNA-Seq, microRNA (miRNA)-Seq, and DNA methylation (methyl)-Seq data on biopsy samples from 331 individuals from across the range of glucose tolerance: 124 normal glucose tolerance (NGT), 77 impaired glucose tolerance (IGT), 44 impaired fasting glucose (IFG), and 86 newly-diagnosed T2Ds. Participants completed two study visits, two weeks apart. First visits comprised most of the clinical phenotyping, including four-point OGTT (fasting, and 30, 60, and 120 minute post-load); BMI, WHR; lipids; blood pressure; and many other variables. Participants also completed FUSION health history, medication, and lifestyle questionnaires. At second visit, we obtained ~250mg <i>vastus lateralis</i> skeletal muscle, ~750mg abdominal subcutaneous adipose, and a ~5x15mm section of abdominal skin. Visits were completed in March 2013. RNA isolation is ongoing in the Collins laboratory at the NIH, RNA and miRNA sequencing at the NIH Intramural Sequencing Center (NISC), and genotyping at the Center for Inherited Disease Research (CIDR). Individual-level data is available here for the 306 individuals who consented to data deposit.</p> <p>To focus on evaluation of gene expression and its regulation in skeletal muscle, we analyzed mRNA extracted from <i>vastus lateralis</i> skeletal muscle obtained from 271 of the 331 individual subjects from Finland, along with genome-wide genotypes. Individual-level data is available here for the 250 subjects who reconsented to the use of their data. Release phs001048.v2.p1 adds muscle data for an additional 42 subjects and data from adipose tissue for 276 subjects. Total RNA was isolated using Trizol extraction in the Collins laboratory at the NIH. The mRNA was poly-A selected, 24-plex libraries were generated using the Illumina TruSeq directional mRNA-seq library protocol and RNA sequencing was performed on HiSeq2000 sequencers using 101bp paired-end reads at NISC. miRNA libraries were prepared from total RNA from 296 muscle and 270 adipose samples, pooled and sequenced 50bp single-end reads on Illumina HiSeq2500. Data for 272 muscle and 251 adipose samples are available here for individuals with consent for data deposit. DNA was extracted from blood in the Collins laboratory, and genotyping on the Illumina Omni2.5M array was performed at CIDR. Genotypes were imputed using the HRC 2016 reference panel. In order to assess regions of open chromatin in skeletal muscle, we obtained muscle tissue from a commercial provider to perform ATAC-seq; these samples were sequenced at the University of Michigan DNA Sequencing Core.</p> <p>Greater than 90% of the approximately 80 loci associated with T2D and the 100s of loci associated with T2D-related traits (glucose and insulin, anthropometrics, lipids) through genome-wide association studies occur in non-coding regions, suggesting a strong regulatory component to disease susceptibility. Regulatory element activity is often tissue-specific, which further complicates discovery of the causal/functional variation. Therefore, there is a critical need to understand the full spectrum of genetic variation and regulatory element usage in T2D-relevant tissues. To that end, this study contains whole genome sequence and whole genome bisulfite sequence, and/or Illumina MethylationEPIC Array data, of two tissues relevant to T2D: skeletal muscle and adipose tissue from individuals with glucose tolerance categories ranging from normal to T2D, providing a comprehensive survey of both individual genetic variation as well as DNA methylation across different tissues from multiple individuals.</p>
| phs001048 | dbGaP
Project description:Alternative splicing (AS) is a key regulatory mechanism for the development of different tissues; however, not much is known about changes to alternative splicing during aging. Splicing events may become more frequent and widespread genome-wide as tissues age and the splicing machinery stringency decreases. Using skin, skeletal muscle, bone, thymus and white adipose tissue from wild-type C57BL6/J male mice (4 and 18-months-old), we examined the effect of age on splicing by AS analysis of the differential exon usage of the genome. The results identified a considerable number of AS genes in skeletal muscle, thymus, bone and white adipose tissue between the different age groups (ranging from 27-246 AS genes corresponding to 0.3-3.2% of the total number of genes analyzed). For skin, skeletal muscle and bone we included a later age group (28-month-old) that showed the number of alternatively spliced genes increased with age in all three tissues (P<0.01). Analysis of alternatively spliced genes across all tissues by gene-ontology and pathway analysis identified 158 genes involved in RNA processing. Additional analysis of AS in a mouse model for the premature aging disease Hutchinson-Gilford progeria syndrome was performed. The results show that expression of the mutant protein, progerin, is associated with impaired developmental splicing. As progerin accumulates the number of genes with AS increases compared to in wild-type skin. Our results indicate the existence of a mechanism for increased AS during aging in several tissues, emphasizing that AS has a more important role in the aging process than previously known.
2015-11-30 | GSE74274 | GEO