AI Article Synopsis
- PM exposure increases the risk of vascular dysfunction, but the exact biological response of endothelial cells to PM is still not fully understood.
- In a study using 4-week-old mice exposed to real airborne PM, bronchial and alveolar damage was observed, and a deficit of Cdk5 led to changes in vasoconstriction and myogenic activity in blood vessels.
- The findings suggest that CDK5 is crucial for endothelial cell growth, migration, and response to PM, indicating its role as a sensor for vascular endothelial responses.
Article Abstract
PM infiltrates into circulation and increases the risk of systemic vascular dysfunction. As the first-line barrier against external stimuli, the molecular mechanism of the biological response of vascular endothelial cells to PM exposure remains unclear. In this study, 4-week-old mice were exposed to Hangzhou 'real' airborne PM for 2 months and were found to display bronchial and alveolar damage. Importantly, in the present study, we have demonstrated that Cdk5 deficit induced peripheral vasoconstriction through angiotensin II type 1 receptor under angiotensin II stimulation in Cdh5-cre;Cdk5 mice. In the brain, Cdk5 deficit increased the myogenic activity in the medullary arterioles under external pressure. On the other hand, no changes in cerebral blood flow and behavior patterns were observed in the Cdh5-cre;Cdk5 mice exposed to PM. Therefore, our current findings indicate that CDK5 plays an important role in endothelium cell growth, migration, and molecular transduction, which is also a sensor for the response of vascular endothelial cells to PM.
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| http://dx.doi.org/10.1016/j.ecoenv.2021.112314 | DOI Listing |
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