Toxicity in hematopoietic stem cells from bone marrow and peripheral blood in mice after benzene exposure: Single-cell transcriptome sequencing analysis

Sun, Rongli; Xu, Kai; Ji, Shuangbin; Pu, Yunqiu; Yu, Linling; Yin, Lihong; Zhang, Juan; Pu, Yuepu

doi:10.1016/j.ecoenv.2020.111490

Cited by 25 publications

(5 citation statements)

References 46 publications

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“…Interestingly, there were 164 common DEGs in both BM and peripheral HSCs, out of which 53 genes were co-controlled in both types of HSCs. Successive pathway investigation of these 53 genes suggested that the most important pathways implicated neutrophil degranulation and CD93 contained in the core of the network of the 53 genes, which are recognized to control leukemia stem cell quiescence and self-renewal [ 135 ].…”

Section: Epigenetics Hematological Neoplasms and Benzenementioning

confidence: 99%

Epigenetic Effects of Benzene in Hematologic Neoplasms: The Altered Gene Expression

Spatari

Allegra

Carrieri

et al. 2021

Cancers

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Benzene carcinogenic ability has been reported, and chronic exposure to benzene can be one of the risk elements for solid cancers and hematological neoplasms. Benzene is acknowledged as a myelotoxin, and it is able to augment the risk for the onset of acute myeloid leukemia, myelodysplastic syndromes, aplastic anemia, and lymphomas. Possible mechanisms of benzene initiation of hematological tumors have been identified, as a genotoxic effect, an action on oxidative stress and inflammation and the provocation of immunosuppression. However, it is becoming evident that genetic alterations and the other causes are insufficient to fully justify several phenomena that influence the onset of hematologic malignancies. Acquired epigenetic alterations may participate with benzene leukemogenesis, as benzene may affect nuclear receptors, and provoke post-translational alterations at the protein level, thereby touching the function of regulatory proteins, comprising oncoproteins and tumor suppressor proteins. DNA hypomethylation correlates with stimulation of oncogenes, while the hypermethylation of CpG islands in promoter regions of specific tumor suppressor genes inhibits their transcription and stimulates the onset of tumors. The discovery of the systems of epigenetic induction of benzene-caused hematological tumors has allowed the possibility to operate with pharmacological interventions able of stopping or overturning the negative effects of benzene.

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Section: Epigenetics Hematological Neoplasms and Benzenementioning

confidence: 99%

Epigenetic Effects of Benzene in Hematologic Neoplasms: The Altered Gene Expression

Spatari

Allegra

Carrieri

et al. 2021

Cancers

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“…95 In addition, cadmium exposure decreased the abundance of CD14 + monocyte subset in peripheral blood mononuclear cells. 96 Sun et al 97 examined transcriptomic alternations in bone marrow hematopoietic stem cells and peripheral blood hematopoietic stem cells of male mice under benzene exposure and revealed that transcriptional misregulation in cancer and hematopoietic cell lineage are important pathways of altered in bone marrow hematopoietic stem cells, while hematopoietic cell lineage and leukocyte transendothelial migration are important pathways altered in peripheral blood hematopoietic stem cells.…”

Section: Toxicogenomics Technologymentioning

confidence: 99%

Advances in Single-Cell Toxicogenomics in Environmental Toxicology

Liu

Chen

et al. 2022

Environ. Sci. Technol.

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The toxicity evaluation system of environmental pollutants has undergone numerous changes due to the application of new technologies. Single-cell toxicogenomics is rapidly changing our view on environmental toxicology by increasing the resolution of our analysis to the level of a single cell. Applications of this technology in environmental toxicology have begun to emerge and are rapidly expanding the portfolio of existing technologies and applications. Here, we first summarized different methods involved in single-cell isolation and amplification in single-cell sequencing process, compared the advantages and disadvantages of different methods, and analyzed their development trends. Then, we reviewed the main advances of single-cell toxicogenomics in environmental toxicology, emphatically analyzed the application prospects of this technology in identifying the target cells of pollutants in early embryos, clarifying the heterogeneous response of cell subtypes to pollutants, and finding pathogenic bacteria in unknown microbes, and highlighted the unique characteristics of this approach with high resolution, high throughput, and high specificity by examples. We also offered a prediction of the further application of this technology and the revolution it brings in environmental toxicology. Overall, these advances will provide practical solutions for controlling or mitigating exogenous toxicological effects that threaten human and ecosystem health, contribute to improving our understanding of the physiological processes affected by pollutants, and lead to the emergence of new methods of pollution control.

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“…Sun et al [111] found an altered activity of mitogen-activated protein kinase (MAPK) pathway with an upregulation of 5 genes and 32 downregulated genes related to this pathway in exposed mice HSCs, suggesting that alteration of the MAPK pathway may contribute to the benzene-related toxic effects. They also valued the genetic setting in peripheral blood HSCs (PBMCs) of the same animal model exposed to benzene and observed a significant change in the expression of 3 genes (Cd7, Cd9, and Cd22) that are related to the differentiation of lymphoid stem cells into T and B lymphocytes.…”

Section: Immunological Aspectsmentioning

confidence: 99%

Effects of Benzene: Hematological and Hypersensitivity Manifestations in Resident Living in Oil Refinery Areas

Cordiano

Papa

Cicero

et al. 2022

Toxics

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Literature is teeming with publications on industrial pollution. Over the decades, the main industrial pollutants and their effects on human health have been widely framed. Among the various compounds involved, benzene plays a leading role in the onset of specific diseases. Two systems are mainly affected by the adverse health effects of benzene exposure, both acute and chronic: the respiratory and hematopoietic systems. The most suitable population targets for a proper damage assessment on these systems are oil refinery workers and residents near refining plants. Our work fits into this area of interest with the aim of reviewing the most relevant cases published in the literature related to the impairment of the aforementioned systems following benzene exposure. We perform an initial debate between the two clinical branches that see a high epidemiological expression in this slice of the population examined: residents near petroleum refinery areas worldwide. In addition, the discussion expands on highlighting the main immunological implications of benzene exposure, finding a common pathophysiological denominator in inflammation, oxidative stress, and DNA damage, thus helping to set the basis for an increasingly detailed characterization aimed at identifying common molecular patterns between the two clinical fields discussed.

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Toxicity in hematopoietic stem cells from bone marrow and peripheral blood in mice after benzene exposure: Single-cell transcriptome sequencing analysis

Cited by 25 publications

References 46 publications

Epigenetic Effects of Benzene in Hematologic Neoplasms: The Altered Gene Expression

Epigenetic Effects of Benzene in Hematologic Neoplasms: The Altered Gene Expression

Advances in Single-Cell Toxicogenomics in Environmental Toxicology

Effects of Benzene: Hematological and Hypersensitivity Manifestations in Resident Living in Oil Refinery Areas

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