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Identification of the Hub Genes Linked to Lead (IV)-Induced Spleen Toxicity Using the Rat Model
Bing Yang1,2, Zhongyuan Wang1, Zhongze Hu1
1College of Animal Science, Anhui Science and Technology University, Bengbu, 233100, China.
Abstract:
Exposure to lead (Pb) has harmful effects on the organs of both humans and animals, particularly the spleen. However, the precise mechanisms through which Pb (IV) exposure leads to spleen toxicity remain unclear. Hence, this study aimed to identify the key genes and signaling pathways involved in spleen toxicity caused by Pb (IV) incubation. We obtained the dataset GSE59925 from the Gene Expression Omnibus, which included spleen samples treated with lead tetraacetate (PbAc4) as well as control samples on the 1st and 5th day. Through differential expression analysis, we identified 607 and 704 differentially expressed genes (DEGs) in the spleens on the 1st and 5th day following PbAc4 treatment, respectively, with 245 overlapping DEGs between the two time points. Gene ontology analysis revealed that the commonly shared DEGs were primarily involved in signal transduction, drug response, cell proliferation, adhesion, and migration. Pathway analysis indicated that the common DEGs were primarily associated with MAPK, TNF, cAMP, Hippo, and TGF-β signaling pathways. Furthermore, we identified the hub genes such as CXCL10, PARP1, APOE, and VDR contributing to PbAc4-induced spleen toxicity. This study enhances our understanding of the molecular mechanisms underlying Pb (IV) toxicity in the spleen.
Insights
Lead exposure harms the spleen, but mechanisms are unclear. This study identified key genes and pathways, like MAPK and TNF signaling, involved in lead tetraacetate (PbAc4)-induced spleen toxicity.
Area of Science:
- Toxicology
- Molecular Biology
- Genomics
Background:
- Lead (Pb) exposure poses significant health risks, particularly affecting the spleen.
- The exact molecular mechanisms of lead (IV) tetraacetate (PbAc4) induced spleen toxicity are not fully understood.
Purpose of the Study:
- To elucidate the key genes and signaling pathways implicated in spleen toxicity following PbAc4 exposure.
- To identify molecular targets for understanding and potentially mitigating lead-induced spleen damage.
Main Methods:
- Utilized Gene Expression Omnibus dataset GSE59925, comparing PbAc4-treated and control spleen samples at day 1 and day 5.
- Performed differential gene expression analysis (DEGs), Gene Ontology (GO) analysis, and pathway analysis.
- Identified overlapping DEGs and hub genes critical for PbAc4 toxicity.
Main Results:
- Identified 607 and 704 DEGs at day 1 and day 5, with 245 overlapping DEGs.
- Common DEGs are enriched in signal transduction, cell proliferation, adhesion, and migration.
- Key pathways include MAPK, TNF, cAMP, Hippo, and TGF-β signaling; hub genes include CXCL10, PARP1, APOE, and VDR.
Conclusions:
- This research reveals critical molecular players and pathways in PbAc4-induced spleen toxicity.
- Findings contribute to a deeper understanding of lead's detrimental effects on the spleen at a molecular level.
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