Microplastics accelerates the premature aging of blood vessels though ROS-mediated CDK5 signaling pathway

Abstract

Abstract Background Microplastic has become a kind of pollutant widely existing in soil, atmosphere, fresh water and marine environment. At present, microplastics have been found in many tissues and organs of organisms. Research shows that as a new environmental pollutant, microplastics has shown a health hazard to human and animal. Aging and aging-related diseases are major social and medical problems facing the world. However, up to now, the effect of microplastic exposure on premature aging of blood vessels has not been evaluated. Therefore, we investigated the health damage of microplastics to blood vessels in vivo and in vitro experiments. Methods ELISA, indirect immunofluorescence, SiRNA, laser confocal microscopy, and Flow cytometry were performed to evaluate the effect of microplastics on premature aging of blood vessels. Results In vitro experiments, we found that microplastics can internalize into vascular cells, and the internalized microplastics cause damage to organelles. Further biochemical experiments showed that microplastics stimulation caused the premature aging of blood vessels by detecting a series of aging markers. Further mechanism research indicates that microplastics could increase ROS level of mitochondria mediated by calcium overload, and then ROS leads to the LaminA degradation by CDK5 mediation, further resulting in genomic instability, thus finally causing the aging of vascular cells/tissues. In vivo model, we found that microplastics induced aging damage on vascular tissue, the expression of aging maker molecules were significantly increased. Furthermore, the level of inflammation and oxidative stress was also significantly increased. Conclusion In summary, in this work, we evaluated the effect of microplastic exposure on premature aging of blood vessels, and we also revealed the molecular mechanism by which microplastics cause premature aging of the cardiovascular system.