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Unveiling the Mechanisms of Bone Marrow Toxicity Induced by Lead Acetate Exposure

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Abstract

Lead (Pb), a widespread heavy metal, causes severe toxicity in human and animal organs (e.g., bone marrow), whereas the mechanisms of the bone marrow toxicity induced by Pb exposure are unclear. Hence, this study was designed to reveal the hub genes involved in Pb-induced bone marrow toxicity. GSE59894 dataset obtained from Gene Expression Omnibus (GEO) was composed of lead acetate (PbAc2)-treated and control bone marrow samples. Totally 120 and 85 differentially expressed genes (DEGs) were identified on the 1st day, while 153 and 157 DEGs on the 3rd day in the bone marrow treated with 200 and 600 mg/kg of PbAc2, respectively. Notably, a total of 28 and 32 overlapping DEGs were identified in the bone marrow on the 1st and 3rd day treated with PbAc2, respectively. Biological process analysis suggested that the common DEGs were primarily participated in cell differentiation, the response to drug, xenobiotic stimulus, and organic cyclic compound. Pathway analysis demonstrated that the overlapping DEGs were primarily linked to PI3K-Akt, TGF-β, MAPK, and osteoclast differentiation signaling pathways. Moreover, the hub genes, including PLD2, DAPK1, ALB, TNF, FOS, CDKN1A, and TGFB3, might contribute to PbAc2-induced bone marrow toxicity. Overall, our study offers an important insight into the molecular mechanisms of Pb-induced bone marrow toxicity.

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All data of the present article are included in Supplementary Information files or in the main text.

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Funding

This study was supported by The Open Project of Anhui Province Key Laboratory of Embryo Development and Reproductive Regulation (No. FSKFKT011), Talent Introduction Program of Anhui Science and Technology University (No. DKYJ202003), The Open Project of Anhui Province Key Laboratory of Wetland Ecosystem Protection and Restoration (No. AHZDSYS2019-01), Natural Science Foundation of Anhui Provincial Education Department (No. KJ2020A0083) and The Open Project of Longyan University & Fujian Provincial Key Laboratory for Prevention and Control of Animal Infectious Diseases and Biotechnology (No. ZDSYS2020004).

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XF Li designed the study, prepared the figures and analyzed the results. B Yang prepared the tables and wrote the manuscript. All authors reviewed the manuscript.

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Correspondence to Xiaofeng Li.

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Supplementary Information

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Supplementary file1The DEGs identified on the 1st day treated with PbAc200 (XLSX 21 KB)

Supplementary file2 The DEGs identified on the 1st day treated with PbAc600 (XLSX 17 KB)

Supplementary file3 The DEGs identified on the 1st day between PbAc200 and PbAc600 (XLSX 12 KB)

Supplementary file4 The DEGs identified on the 3rd day treated with PbAc200 (XLSX 23 KB)

Supplementary file5 The DEGs identified on the 3rd day treated with PbAc600 (XLSX 26 KB)

Supplementary file6 The DEGs identified on the 3rd day between PbAc200 and PbAc600 exposure (XLSX 11 KB)

Supplementary file7 The overlapping DEGs identified on the 1st day treated with PbAc200 and PbAc600 (XLSX 10 KB)

Supplementary file8 The overlapping DEGs identified on the 3rd day treated with PbAc200 and PbAc600 (XLSX 13 KB)

Supplementary file9 The overlapping DEGs identified on the 1st and 3rd day treated with PbAc200 (XLSX 10 KB)

12011_2023_3733_MOESM10_ESM.xlsx

Supplementary file10 The overlapping DEGs identified in the bone marrow on the 1st and 3rd day treated with PbAc600 (XLSX 10 KB)

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Yang, B., Li, X. Unveiling the Mechanisms of Bone Marrow Toxicity Induced by Lead Acetate Exposure. Biol Trace Elem Res 202, 1041–1066 (2024). https://doi.org/10.1007/s12011-023-03733-w

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