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Updated: Jun 10, 2025

In Ovo Electroporations of HH Stage 10 Chicken Embryos
Published on: November 1, 2007
Unveiling the hub genes associated with ochratoxin A-induced hepatotoxicity in broiler chickens
Xiaofeng Li1, Zhongyuan Wang1, Shujuan Wang1
1College of Animal Science, Anhui Science and Technology University, Fengyang, China.
Abstract:
Ochratoxin A (OTA) widely exists in raw food and feed materials and can induce liver damage and toxicity. However, the mechanisms of OTA-induced hepatotoxicity were largely unknown. Thus, our study aimed to uncover the vital genes relevant to OTA-induced hepatotoxicity in broiler chickens. Gene expression data of chicken embryo primary hepatocytes (CEPHs) in OTA-treated and control groups were obtained from the GEO database. Totally 1407 differentially expressed genes (DEGs) were selected, of which 850 and 557 genes were up- and downregulated in OTA-treated CEPHs. Gene ontology (GO) enrichment revealed that the DEGs were in connection with various biological processes, such as signal transduction, extracellular matrix organization, axon guidance, cell division, cholesterol homeostasis, proteolysis, microtubule cytoskeleton organization, and chromosome segregation. Pathway enrichment showed that the DEGs were related to metabolic pathways, ferroptosis, calcium, FoxO, Wnt, cell cycle, apoptosis, calcium, and cell adhesion molecules signaling pathways. Furthermore, the hub genes, including CDK1, DLGAP5, KIF2C, VCL, ITGB3, and ZYX, were identified as hub genes potentially contributing to OTA-induced hepatotoxicity. Taken together, this study provides valuable insights into the mechanisms underlying OTA-induced hepatotoxicity in broiler chickens.
Insights
Ochratoxin A (OTA) causes liver damage in chickens. This study identified key genes like CDK1 and DLGAP5 involved in OTA-induced hepatotoxicity, revealing crucial biological pathways.
Area of Science:
- Animal Science
- Toxicology
- Molecular Biology
Background:
- Ochratoxin A (OTA) is a common contaminant in food and feed, known to cause liver toxicity.
- The precise molecular mechanisms of OTA-induced hepatotoxicity in broiler chickens remain largely unelucidated.
Purpose of the Study:
- To identify critical genes and pathways associated with OTA-induced hepatotoxicity in broiler chickens.
- To elucidate the molecular mechanisms underlying OTA toxicity in avian species.
Main Methods:
- Differential gene expression analysis of chicken embryo primary hepatocytes (CEPHs) exposed to OTA.
- Gene Ontology (GO) and pathway enrichment analyses were performed on differentially expressed genes (DEGs).
- Identification of hub genes using network analysis.
Main Results:
- 1407 DEGs were identified, with 850 upregulated and 557 downregulated in OTA-treated CEPHs.
- Enrichment analyses highlighted involvement in signal transduction, cell division, cholesterol homeostasis, ferroptosis, and cell cycle pathways.
- Key hub genes, including CDK1, DLGAP5, KIF2C, VCL, ITGB3, and ZYX, were identified as potentially crucial for OTA-induced liver damage.
Conclusions:
- This study provides significant insights into the molecular mechanisms of OTA-induced hepatotoxicity in broiler chickens.
- The identified genes and pathways offer potential targets for mitigating OTA toxicity in poultry.
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