Endothelial dysfunction and transcriptome aberration in mouse aortas induced by black phosphorus quantum dots and nanosheets

Black phosphorus (BP) nanomaterials have shown great potential in versatile applications including biomedicine and potentially interact with vessel walls following intravenous injection in biomedical usage or environmental exposure. However, it remains unknown whether the exposure to BP nanomaterials induces alterations of the endothelium and further vascular injury. Herein, the endothelial function of human umbilical vein endothelial cells (HUVECs) and the structure and transcriptome of C57BL/6 mouse aortas are evaluated after the exposure to BP quantum dots (BPQDs) and nanosheets (BPNSs). BPNSs with irregular shapes and larger lateral size are more prone to inhibit in vitro angiogenesis at non-cytotoxic concentrations and markedly trigger platelet adhesion to HUVECs compared to BPQDs. Decreased nitric oxide (NO) production resulting from endothelial NO synthase (eNOS) dysregulation is involved in the BP-induced endothelial dysfunction. Both BPQDs and BPNSs at 0.8 and 6.4 mu g mL(-1) inhibit eNOS enzymatic activity through dephosphorylation of eNOS-Ser(1177) and phosphorylation of eNOS-Thr(495), but unlike BPQDs, BPNSs also downregulate eNOS expression. Despite no pathological damage in the structure of mouse aortas, BPQDs and BPNSs trigger aberration of aortic transcriptome involved in vasoconstriction abnormality, metabolic disturbance, and immune perturbation. This study demonstrates the adverse effect of BP nanomaterials on vasculature, and suggests that the morphological attribute of BP plays a crucial role in the vascular risks.

Automated summary

In this study, it was found that black phosphorus nanomaterials have adverse effects on vasculature, with BPNSs being more likely to cause endothelial dysfunction and platelet adhesion. The impact on eNOS also differs between BPQDs and BPNSs. Although there was no significant structural damage in the mouse aortas, both BPQDs and BPNSs triggered aberrations in the aortic transcriptome, involving vasoconstriction abnormalities, metabolic disturbances, and immune perturbations.