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Series GSE239570 Query DataSets for GSE239570
Status Public on Aug 03, 2023
Title CPT1B regulates goat intramuscular preadipocyte lipid deposition through p38MAPK signaling pathway
Organism Capra hircus
Experiment type Expression profiling by high throughput sequencing
Summary 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.
 
Overall design Differentially expressed genes were detected by RNA-seq sequencing in goat intramuscular adipocytes from knockdown CPT1B (si-CPT1B) and negative control (NC).
 
Contributor(s) Wang Y, Zhu J, Huang L
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BioProject PRJNA978364
Submission date Jul 28, 2023
Last update date Aug 03, 2023
Contact name Yinggui Wang
E-mail(s) YingguiWang326@outlook.com
Phone 18788705310
Organization name Qinghai-Tibetan Plateau Animal Genetic Resource Reservation and Utilization Key Laboratory of Sichuan Province
Lab 2-31
Street address 2-31, Jingwenyuan, South District, Airport Campus, Southwest University for Nationalities, Chengdu, Sichuan
City chengdu
State/province sichuan
ZIP/Postal code 610000
Country China
 
Platforms (1)
GPL21299 Illumina NextSeq 500 (Capra hircus)
Samples (8)
GSM7667401 intramuscular adipocytes, si-CPT1B-1
GSM7667402 intramuscular adipocytes, si-CPT1B-2
GSM7667403 intramuscular adipocytes, si-CPT1B-3

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE239570_cpt1bFPKM.csv.gz 595.0 Kb (ftp)(http) CSV
GSE239570_cpt1bcount.csv.gz 147.4 Kb (ftp)(http) CSV
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Raw data are available in SRA
Processed data are available on Series record

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