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Peer-reviewedCC BY-NC-NDEnvironment & health (Washington, D.C.)

Single-Cell Transcriptomic Profiling of Human Blood Vessel Organoids Exposed to 6‑Chloronicotinic Acid.

  • Siyi Wang1
  • Xianghui Wang2
  • Kailun Wang2
  • Shi Tang3
  • Xia Sheng2
  • Shunqing Xu4
  • Yahang Lin1
  • Mingxi Zhang5
  • Fengzhen Cui6
6 affiliations
  1. 1Department of Neurology, Wuhan Fourth Hospital, Wuhan 430033, China.
  2. 2Institute of Biomedical Research, School of Life and Health Sciences, Hainan University, Haikou 570228, China.
  3. 3Department of Research Development, Hainan University, Haikou 570228, China.
  4. 4School of Environmental Science and Engineering, Hainan University, Haikou 570228, China.
  5. 5Department of Cardiovascular Disease, Wuhan Hospital of Traditional Chinese Medicine, Wuhan 430060, China.
  6. 6School of Public Health, Guangdong Medical University, Dongguan 523808, China.
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Abstract

6-Chloronicotinic acid (6-ClNA) is a major metabolite of chloropyridinyl neonicotinoids in humans; however, its toxic effect on blood vessel development remains to be understood. In this study, we utilized a humanized blood vessel organoid (hBVO) model and single-cell transcriptomics technology to investigate the impact of 6-ClNA exposure on hBVO development. Morphologically, 6-ClNA did not significantly alter the growth of hBVO throughout 20 days of culture. Interestingly, single-cell transcriptomic analyses revealed that 6-ClNA-treated hBVOs exhibited significant imbalance in cell subpopulation homeostasis, including impaired endothelial cell function and abnormal proliferation of vascular smooth muscle cells. This was echoed by the morphological changes in the aortic arch and abdominal aorta of mice after acute exposure to 6-ClNA. Enrichment analysis showed that 6-ClNA exposure affected critical biological processes in a cell-type-specific manner, such as vascular developmental signaling, cellular energy metabolism, protein homeostasis, and hemodynamic responses. In addition, trajectory analysis suggested that 6-ClNA altered the differentiation trajectory of vascular progenitors. Together, our study profiles the toxicity of 6-ClNA on blood vessel development in a humanized 3D model at single-cell resolution, which provides important and detailed evidence for understanding the potential risk of early life exposure to chloropyridinyl neonicotinoids.

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Cite

BibTeXRIS
BibTeX
@article{wang2026singlecell,
  title = {{Single-Cell Transcriptomic Profiling of Human Blood Vessel Organoids Exposed to 6‑Chloronicotinic Acid.}},
  author = {Siyi Wang and Xianghui Wang and Kailun Wang and Shi Tang and Xia Sheng and Shunqing Xu and Yahang Lin and Mingxi Zhang and Fengzhen Cui},
  journal = {Environment \& health (Washington, D.C.)},
  year = {2026},
  month = jun,
  doi = {10.1021/envhealth.6c00026},
  url = {https://europepmc.org/article/MED/42903721},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Single-Cell Transcriptomic Profiling of Human Blood Vessel Organoids Exposed to 6‑Chloronicotinic Acid.
AU  - Siyi Wang
AU  - Xianghui Wang
AU  - Kailun Wang
AU  - Shi Tang
AU  - Xia Sheng
AU  - Shunqing Xu
AU  - Yahang Lin
AU  - Mingxi Zhang
AU  - Fengzhen Cui
PY  - 2026
DA  - 2026/06/03
JO  - Environment & health (Washington, D.C.)
DO  - 10.1021/envhealth.6c00026
UR  - https://europepmc.org/article/MED/42903721
AB  - 6-Chloronicotinic acid (6-ClNA) is a major metabolite of chloropyridinyl neonicotinoids in humans; however, its toxic effect on blood vessel development remains to be understood. In this study, we utilized a humanized blood vessel organoid (hBVO) model and single-cell transcriptomics technology to investigate the impact of 6-ClNA exposure on hBVO development. Morphologically, 6-ClNA did not significantly alter the growth of hBVO throughout 20 days of culture. Interestingly, single-cell transcriptomic analyses revealed that 6-ClNA-treated hBVOs exhibited significant imbalance in cell subpopulation homeostasis, including impaired endothelial cell function and abnormal proliferation of vascular smooth muscle cells. This was echoed by the morphological changes in the aortic arch and abdominal aorta of mice after acute exposure to 6-ClNA. Enrichment analysis showed that 6-ClNA exposure affected critical biological processes in a cell-type-specific manner, such as vascular developmental signaling, cellular energy metabolism, protein homeostasis, and hemodynamic responses. In addition, trajectory analysis suggested that 6-ClNA altered the differentiation trajectory of vascular progenitors. Together, our study profiles the toxicity of 6-ClNA on blood vessel development in a humanized 3D model at single-cell resolution, which provides important and detailed evidence for understanding the potential risk of early life exposure to chloropyridinyl neonicotinoids.
SN  - 2833-8278
ER  -