Ambient fine particulate matter exposure induces reversible cardiac dysfunction and fibrosis in juvenile and older female mice

CORC > 生态环境研究中心 > 中国科学院生态环境研究中心 > 环境化学与生态毒理学国家重点实验室

	Ambient fine particulate matter exposure induces reversible cardiac dysfunction and fibrosis in juvenile and older female mice
	Qin, Guohua; Xia, Jin; Zhang, Yingying; Guo, Lianghong; Chen, Rui; Sang, Nan
刊名	PARTICLE AND FIBRE TOXICOLOGY
	2018-06-25
卷号	15 页码:-
关键词	Particulate matter Cardiac Fibrosis Reversible Different age
ISSN号	1743-8977
文献子类	Article
英文摘要	Background: Cardiovascular disease is the leading cause of mortality in the advanced world, and age is an important determinant of cardiac function. The purpose of the study is to determine whether the PM2.5-induced cardiac dysfunction is age-dependent and whether the adverse effects can be restored after PM2.5 exposure withdrawal. Methods: Female C57BL/6 mice at different ages (4-week-old, 4-month-old, and 10-month-old) received oropharyngeal aspiration of 3 mg/kg b.w. PM2.5 every other day for 4 weeks. Then, 10-month-old and 4-week-old mice were exposed to PM2.5 for 4 weeks and withdrawal PM2.5 1 or 2 weeks. Heart rate and systolic blood pressure were measured using a tailcuff system. Cardiac function was assessed by echocardiography. Left ventricles were processed for histology to assess myocardial fibrosis. ROS generation was detected by photocatalysis using 2', 7'-dichlorodihydrofluorescein diacetate (DCFHDA). The expression of cardiac fibrosis markers (Col1a1, Col3a1) and possible signaling molecules, including NADPH oxidase 4 (NOX-4), transforming growth factor beta 1 (TGF beta 1), and Smad3, were detected by qPCR and/or Western blot. Results: PM2.5 exposure induced cardiac diastolic dysfunction of mice, elevated the heart rate and blood pressure, developed cardiac systolic dysfunction of 10-month-old mice, and caused fibrosis in both 4-week-old and 10-month-old mice. PM2.5 exposure increased the expression of Col1a1, Col3a1, NOX-4, and TGF beta 1, activated Smad3, and generated more reactive oxygen species in the myocardium of 4-week-old and 10-month-old mice. The withdrawal from PM2.5 exposure restored blood pressure, heart rate, cardiac function, expression of collagens, and malonaldehyde (MDA) levels in hearts of both 10-month-old and 4-week-old mice. Conclusion: Juvenile and older mice are more sensitive to PM2.5 than adults and suffer from cardiac dysfunction. PM2.5 exposure reversibly elevated heart rate and blood pressure, induced cardiac systolic dysfunction of older mice, and reversibly induced fibrosis in juvenile and older mice. The mechanism by which PM2.5 exposure resulted in cardiac lesions might involve oxidative stress, NADPH oxidase, TGF beta 1, and Smad-dependent pathways.
内容类型	期刊论文
源URL	[http://ir.rcees.ac.cn/handle/311016/40872]
专题	生态环境研究中心_环境化学与生态毒理学国家重点实验室
推荐引用方式 GB/T 7714	Qin, Guohua,Xia, Jin,Zhang, Yingying,et al. Ambient fine particulate matter exposure induces reversible cardiac dysfunction and fibrosis in juvenile and older female mice[J]. PARTICLE AND FIBRE TOXICOLOGY,2018,15:-.
APA	Qin, Guohua,Xia, Jin,Zhang, Yingying,Guo, Lianghong,Chen, Rui,&Sang, Nan.(2018).Ambient fine particulate matter exposure induces reversible cardiac dysfunction and fibrosis in juvenile and older female mice.PARTICLE AND FIBRE TOXICOLOGY,15,-.
MLA	Qin, Guohua,et al."Ambient fine particulate matter exposure induces reversible cardiac dysfunction and fibrosis in juvenile and older female mice".PARTICLE AND FIBRE TOXICOLOGY 15(2018):-.