Transcriptome modifications in the porcine intramuscular adipocytes during differentiation and exogenous stimulation with TNF-alpha and serotonin
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ABSTRACT:
PROVIDER: PRJNA594382 | ENA |
REPOSITORIES: ENA
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Project description:Adipocytes are dynamic cells that have critical functions to maintain body energy homeostasis. Function of adipocyte is affected by adipogenic differentiation, and exogenous stimulation of biochemical factors such as serotonin and TNF-. Serotonin (5-hydroxytriptamine, 5-HT) is a biogenic monoamine, which known to be involved in lipid metabolism in adipocytes. The TNF- is a proinflammatory cytokines involved in adipocyte biology. Here we investigated the global transcriptome alterations of porcine intramuscular adipocytes at undifferentiated preadipocyte, differentiated adipocytes state, and adipocytes after stimulation with serotonin and TNF- for 12 h by using Agilent’s Porcine (V2) one-color Gene Expression Microarray 4 × 44. Transcriptome analysis revealed that the expression of 443, 261, and 249 genes were altered after differentiation, and after serotonin and TNF- stimulation, respectively. Differentiation process of adipocytes are found to be involved with expression changes of APP, HNF4A, ESR1, EGR1, SRC, HNF1A, FN1, ALB, STAT3, CBL, CEBPB, AR, FOS, CFTR, PAN2, PTPN6, VDR, PPARG, STAT5A and NCOA3 genes which are enriched in the ‘PPAR signaling pathway’ and ‘insulin resistance pathway’. Dose-dependent serotonin stimulation resulted in a decreased fat accumulation in the adipocytes as well as decreased adipocyte proliferation. Serotonin-induced differentially expressed genes in adipocytes were participated in the significant enrichment of GPCR ligand-binding, Cell chemotaxis, blood coagulation and complement pathways, metabolism of lipid and lipoproteins, regulation of lipid metabolism by PPARA; and lipid digestion, mobilization and transport pathways. TNF-α-induced transcriptional modification follows the similar trend, and alteration of many genes shared between both serotonin- and TNF-α stimulations. Our results provide new insights of transcriptome modifications associated with adipogenesis, and exogenous stimulation of serotonin- and TNF- to the porcine intramuscular adipocytes.
2020-02-27 | GSE141695 | GEO
Project description:Adipocytes are dynamic cells that have critical functions to maintain body energy homeostasis. Adipocyte physiology is affected by the adipogenic differentiation, cell program, as well as by the exogenous stimulation of biochemical factors, such as serotonin and TNF-?. In this work, we investigated the global transcriptome modifications when porcine intramuscular preadipocyte (PIP) was differentiated into porcine mature adipocyte (pMA). Moreover, we studied transcriptome changes in pMA after stimulation with serotonin or TNF-? by using a microarray approach. Transcriptome analysis revealed that the expression of 270, 261, and 249 genes were modified after differentiation, or after serotonin and TNF-? stimulation, respectively. Expression changes in APP, HNF4A, ESR1, EGR1, SRC, HNF1A, FN1, ALB, STAT3, CBL, CEBPB, AR, FOS, CFTR, PAN2, PTPN6, VDR, PPARG, STAT5A and NCOA3 genes which are enriched in the 'PPAR signaling' and 'insulin resistance' pathways were found in adipocytes during the differentiation process. Dose-dependent serotonin stimulation resulted in a decreased fat accumulation in pMAs. Serotonin-induced differentially expressed genes in pMAs were found to be involved in the significant enrichment of 'GPCR ligand-binding', 'cell chemotaxis', 'blood coagulation and complement', 'metabolism of lipid and lipoproteins', 'regulation of lipid metabolism by PPARA', and 'lipid digestion, mobilization and transport' pathways. TNF-? stimulation also resulted in transcriptome modifications linked with proinflammatory responses in the pMA of intramuscular origin. Our results provide a landscape of transcriptome modifications and their linked-biological pathways in response to adipogenesis, and exogenous stimulation of serotonin- and TNF-? to the pMA of intramuscular origin.
| S-EPMC7013444 | biostudies-literature
Project description:RNA sequencing was performed to obtain a landscape of mRNA, circRNA, lncRNA, and miRNA of bovine intramuscular adipocytes in 4 differentiation periods.
2022-08-31 | GSE185850 | GEO
Project description:To investigate the function lncFABP4 in the regulation of adipogenic differentiation, we overexpressed lncFABP4 in buffalo intramuscular adipocytes
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Project description:To find the differentially and highly expressed circRNAs between the early and late stages of intramuscular adipocytes differentiation. Explored their expression profiles and further predicted their possible interaction relationships. To generated the final circRNA-miRNA interaction network that have valuable functions in adipocyte differentiation.
2023-01-30 | GSE215297 | GEO
Project description:Purpose: In this study, RNA-Seq was performed on intramuscular adipocytes and subcutaneous adipocytes at 0, 2, 4, and 8 days of differentiation to find genes and miRNAs that regulate the differentiation of two types of adipocytes. Methods: High-throughput sequencing was performed with NovaSeq 6000, and 150 paired-end reads were generated.Clean reads were filtered using HISAT2. The StringTie was used to assemble the transcript and calculate fragments per kilobase million mapped reads (FPKM) value. Results: We found 30 genes that mainly regulate the differentiation of subcutaneous adipocytes and 22 genes that mainly regulate the differentiation of subcutaneous intramuscular adipocytes. A total of 17 important candidate differential miRNAs were found, of which 4 miRNAs are believed to play a regulatory role in both types of cells, and 10 and 3 act on lipid deposition in subcutaneous and intramuscular adipocytes, respectively.
2022-06-07 | GSE193607 | GEO
Project description:CPT1B, as the major rate-limiting enzyme for fatty acid β-oxidation, involved in the regulation of adipose tissue lipid deposition, but its role in the regulation of goat intramuscular fat (IMF) remains unclear. Here, we conducted knockdown experiments targeting the CPT1B gene in goat intramuscular preadipocytes, resulting in a significant increase in intracellular triglyceride (TAG) content and lipid droplet accumulation. Conversely, the overexpression of CPT1B led to a significant decrease in intracellular TAG content and lipid droplet accumulation. Mechanistically, through RNA-seq analysis of CPT1B knockdown samples, we identified 285 differentially expressed genes (DEGs), including 71 up-regulated and 214 down-regulated genes. Notably, these DEGs were significantly enriched in various KEGG signaling pathways, such as fatty acid metabolism, focal adhesion, FoxO signaling, PI3K-Akt signaling, and MAPK signaling pathways. Gene Set Enrichment Analysis (GSEA) further confirmed the upregulation of the MAPK signaling pathway upon CPT1B knockdown in adipocytes. In rescue experiments, we demonstrated that the addition of a p38MAPK inhibitor (PD169316) to CPT1B-knockdown adipocytes counteracted the increase in lipid deposition caused by the loss of CPT1B function. These findings suggest that CPT1B inhibits lipid deposition in goat intramuscular preadipocytes via the p38MAPK signaling pathway. In addition, we observed a potential interaction between CPT1B and CPT1A through Protein-Protein Interaction Networks (PPIs). Interestingly, CPT1A exhibited a similar regulatory function to CPT1B, and they both were able to partially restore the changes in lipid deposition induced by each other. This observation supports the hypothesis of synergistic effects between CPT1B and CPT1A. Collectively, our results elucidate the role of CPT1B in the regulation of lipid deposition in goat intramuscular adipocytes through the p38MAPK signaling pathway, providing valuable insights for enhancing the quality of goat intramuscular fat.
2023-08-03 | GSE239570 | GEO
Project description:The meat quality of animal products is closely related to the intramuscular fat content. Aquaglyceroporin (AQP) defines a class of water/glycerol channels that primarily facilitate the passive transport of glycerol and water across biological membranes. In this study, the AQP3 protein of the AQP family was mainly studied in the adipogenic function of intramuscular adipocytes in pigs. Here, we found that AQP3 was increased at both mRNA and protein levels upon adipogenic stimuli in porcine intramuscular adipocytes in vitro. Western blot results showed knockdown of AQP3 by siRNA significantly suppressed the expression of adipogenic genes (PPARγ, aP2, etc.), repressed Akt phosphorylation, as well as reducing lipid accumulation. Furthermore, deletion of AQP3 by siRNA significantly downregulated expression of cell cycle genes (cyclin D, E), and decreased the number of EdU-positive cells as well as cell viability. Collectively, our data indicate that AQP3 is of great importance in both adipogenic differentiation and proliferation in intramuscular adipocytes, providing a potential target for modulating fat infiltration in skeletal muscles.
| S-EPMC7230797 | biostudies-literature
Project description:BACKGROUND:Intramuscular fat (IMF) content is an important factor in porcine meat quality. Previously, we showed that miR-34a was less abundant in liver tissue from pigs with higher backfat thickness, compared to pigs with lower backfat thickness. The purpose of this present study was to explore the role of miR-34a in adipogenesis. RESULT:Bioinformatics analysis identified Acyl-CoA synthetase long chain family member 4 (ACSL4) as a putative target of miR-34a. Using a luciferase reporter assay, we verified that miR-34a binds the ACSL4 mRNA at the 3'UTR. To examine the role of the miR-34a-ACSL4 interaction in IMF deposition in the pig, mRNA and protein expression of the ACSL4 gene was measured in primary intramuscular preadipocytes transfected with miR-34a mimic and inhibitor. Our results showed that ACSL4 is expressed throughout the entire differentiation process in pig preadipocytes, similar to the lipogenesis-associated genes PPAR? and aP2. Transfection with miR-34a mimic reduced lipid droplet formation during adipogenesis, while miR-34a inhibitor increased lipid droplet accumulation. Transfection with miR-34a mimic also reduced the mRNA and protein expression of ACSL4 and lipogenesis genes, including PPAR?, aP2, and SREBP-1C, but increased the expression of steatolysis genes such as ATGL and Sirt1. In contrast, the miR-34a inhibitor had the opposite effect on gene expression. Further, knockdown of ACSL4 decreased lipid droplet accumulation. CONCLUSIONS:Our results support the hypothesis that miR-34a regulates intramuscular fat deposition in porcine adipocytes by targeting ACSL4.
| S-EPMC7073017 | biostudies-literature
Project description:Purpose: In this study, RNA-Seq was performed on intramuscular adipocytes and subcutaneous adipocytes at 0, 2, 4, and 8 days of differentiation to find genes and miRNAs that regulate the differentiation of two types of adipocytes. Method:The clean reads were mapped to the pig reference genome (scrofa. Sscrofa11.1) with perfect matches using Bowtie software. Annotated tRNA, rRNA, snoRNA, and snRNA sequences were filtered out, and conserved miRNAs were identified by the BLAST method against miRBase. The miRDeep2 software was used to predict new miRNAs based on the characteristics of the miRNA precursor hairpin structure. Differential expression analysis of two groups was performed using the DESeq2 R package. Differentially expressed miRNAs (DE-miRNAs) were screened with criterion of fold change > 1.5 and FDR < 0.05 using DESeq2. Target genes of DE-miRNAs were predicted by miRanda and targetscan. Results: We found 30 genes that mainly regulate the differentiation of subcutaneous adipocytes and 22 genes that mainly regulate the differentiation of subcutaneous intramuscular adipocytes. A total of 17 important candidate differential miRNAs were found, of which 4 miRNAs are believed to play a regulatory role in both types of cells, and 10 and 3 act on lipid deposition in subcutaneous and intramuscular adipocytes, respectively.
2022-06-07 | GSE193608 | GEO