Effects of PM2.5 exposure on clock gene BMAL1 and cell cycle in human umbilical vein endothelial cells.
Toxicol Res (Camb)
; 13(1): tfae022, 2024 Feb.
Article
en En
| MEDLINE
| ID: mdl-38419835
ABSTRACT
Background:
Fine particulate matter (PM2.5) exposure has been closely associated with cardiovascular diseases, which are relevant to cell cycle arrest. Brain and muscle aryl-hydrocarbon receptor nuclear translocator-like protein 1 (BMAL1) not only participates in regulating the circadian clock but also plays a role in modulating cell cycle. However, the precise contribution of the circadian clock gene BMAL1 to PM2.5-induced cell cycle change remains unclear. This study aims to explore the impact of PM2.5 exposure on BMAL1 expression and the cell cycle in human umbilical vein endothelial cells (HUVECs).Methods:
HUVECs was exposed to PM2.5 for 24 hours at different concentrations ((0, 12.5, 25, 75 and 100 µg.mL-1) to elucidate the potential toxic mechanism. Following exposure to PM2.5, cell viability, ROS, cell cycle, and the expression of key genes and proteins were detected.Results:
A remarkable decrease in cell viability is observed in the PM2.5-exposed HUVECs, as well as a significant increase in ROS production. In addition, PM2.5-exposed HUVECs have cycle arrest in G0/G1 phase, and the gene expression of p27 is also markedly increased. The protein expression of BMAL1 and the gene expression of BMAL1 are increased significantly. Moreover, the protein expressions of p-p38 MAPK and p-ERK1/2 exhibit a marked increase in the PM2.5-exposed HUVECs. Furthermore, following the transfection of HUVECs with siBMAL1 to suppress BMAL1 expression, we observed a reduction in both the protein and gene expression of the MAPK/ERK pathway in HUVECs exposed to PM2.5.Conclusions:
Overall, our results indicate that PM2.5 exposure significantly upregulates the circadian clock gene expression of BMAL1 and regulates G0/G1 cell cycle arrest in HUVECs through the MAPK/ERK pathway, which may provide new insights into the potential molecular mechanism regarding BMAL1 on PM2.5-induced cardiovascular diseases.
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Colección:
01-internacional
Base de datos:
MEDLINE
Idioma:
En
Revista:
Toxicol Res (Camb)
Año:
2024
Tipo del documento:
Article