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Human Pluripotent Stem Cell Based Developmental Toxicity Assays for Chemical Safety Screening and Systems Biology Data Generation
Published on: June 17, 2015
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Modeling cadmium-induced endothelial toxicity using human pluripotent stem cell-derived endothelial cells
Ling Tang1,2, Jun Su1,2, Ping Liang3,4
1Key Laboratory of combined Multi-organ Transplantation, Ministry of Public Health, the First Affiliated Hospital, Zhejiang University, 310003, Hangzhou, China.
Scientific Reports
|November 3, 2017
Summary
Cadmium exposure causes endothelial cell (EC) death and vascular disease. Inhibiting the P38 or ERK pathways protects against cadmium-induced EC toxicity, offering therapeutic targets for vascular diseases.
Area of Science:
- Toxicology
- Cardiovascular Biology
- Stem Cell Biology
Background:
- Cadmium (Cd) is a toxic heavy metal linked to vascular diseases like atherosclerosis.
- Endothelial cells (ECs) are primary targets of Cd toxicity, leading to dysfunction and death, but mechanisms are unclear.
Purpose of the Study:
- Investigate mechanisms of Cd-induced endothelial toxicity using human pluripotent stem cell-derived ECs (hPSC-ECs).
- Identify key signaling pathways involved in Cd-induced EC apoptosis and dysfunction.
Main Methods:
- Utilized H9 human pluripotent stem cell-derived endothelial cells (H9-ECs) as a model system.
- Assessed CdCl2-induced cytotoxicity, apoptosis, cell structure changes, and transcriptomic profiles.
- Analyzed the role of P38 and ERK signaling pathways in Cd toxicity.
Main Results:
- H9-ECs exhibited structural damage, increased apoptosis, and dysfunction upon CdCl2 exposure.
- CdCl2 treatment induced significant changes in the transcriptomic profile of H9-ECs.
- Inhibition of P38 or ERK signaling pathways ameliorated CdCl2-induced endothelial toxicity.
Conclusions:
- hPSC-ECs serve as a reliable model for studying Cd-induced endothelial toxicity and vascular pathologies.
- P38 and ERK signaling pathways are critical mediators of Cd-induced EC apoptosis and dysfunction.
- Targeting P38 or ERK pathways presents a potential therapeutic strategy for Cd-induced vascular diseases.
