Secondhand Smoke Exposure Reduced the Compensatory Effects of IGF-I Growth Signaling in the Aging Rat Hearts

Wu, Jia; Hsieh, Dennis Jine Yuan; Kuo, Wei Wen; Han, Chien Kuo; Pai, Peiying; Yeh, Yu Lan; Lin, Chien Chung; Padma, V. Vijaya; Day, Cecilia Hsuan; Huang, Chih Yang

doi:10.7150/ijms.12032

Cited by 5 publications

(9 citation statements)

References 34 publications

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“…Similar results were observed with secondhand smoke or lipopolysaccharide (LPS) treatment. Secondhand smoke or LPS induce more cardiac dysfunction, fibrosis, inflammation, and oxidative stress in aged mice than in young mice [ 36 , 37 ]. Aging-associated cardiac abnormalities are manifested as diastolic cardiac dysfunction, cardiac hypertrophy, and fibrosis, as well as impaired contractile function [ 38 , 39 ].…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2018

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BackgroundCardiovascular 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.MethodsFemale 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 tail-cuff 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 β1 (TGFβ1), and Smad3, were detected by qPCR and/ or Western blot.ResultsPM2.5 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 TGFβ1, 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.ConclusionJuvenile 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, TGFβ1, and Smad-dependent pathways.Electronic supplementary materialThe online version of this article (10.1186/s12989-018-0264-2) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

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

et al. 2018

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“…Phosphorylation was unchanged in 14-month-old mice [ 82 ] or 20‒24-month-old rats [ 83 ], and p-STAT3beta was not altered in 24-month-old mice [ 84 ] ( Table 5 ). Three studies showed that the level of STAT3 expression was increased in response to aging in old mice [ 82 ], hamsters [ 72 ] and rats [ 73 ]; however, these findings are limited since the activation (i.e., phosphorylation) was not examined.…”

Section: Effect Of Cardiovascular Risk Factors On Cardiac Stat3 Unmentioning

confidence: 99%

“…Both active and passive (secondhand) smoking are predominant risk factors for coronary heart disease [ 86 ]. We et al reported that passive smoking increases cardiac STAT3 expression in young rats [ 73 ], but does not alter STAT3 expression in hamsters [ 72 ] ( Table 4 ). In aged rats and hamsters exposed to passive smoking, cardiac STAT3 expression showed a tendency to increase [ 72 , 73 ].…”

Section: Effect Of Cardiovascular Risk Factors On Cardiac Stat3 Unmentioning

confidence: 99%

Effects of Cardiovascular Risk Factors on Cardiac STAT3

Pipicz

Demján

Sárközy

et al. 2018

IJMS

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Nuclear, mitochondrial and cytoplasmic signal transducer and activator of transcription 3 (STAT3) regulates many cellular processes, e.g., the transcription or opening of mitochondrial permeability transition pore, and its activity depends on the phosphorylation of Tyr705 and/or Ser727 sites. In the heterogeneous network of cardiac cells, STAT3 promotes cardiac muscle differentiation, vascular element formation and extracellular matrix homeostasis. Overwhelming evidence suggests that STAT3 is beneficial for the heart, plays a role in the prevention of age-related and postpartum heart failure, protects the heart against cardiotoxic doxorubicin or ischaemia/reperfusion injury, and is involved in many cardioprotective strategies (e.g., ischaemic preconditioning, perconditioning, postconditioning, remote or pharmacological conditioning). Ischaemic heart disease is still the leading cause of death worldwide, and many cardiovascular risk factors contribute to the development of the disease. This review focuses on the effects of various cardiovascular risk factors (diabetes, aging, obesity, smoking, alcohol, depression, gender, comedications) on cardiac STAT3 under non-ischaemic baseline conditions, and in settings of ischaemia/reperfusion injury with or without cardioprotective strategies.

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“…Previous studies have shown that exposure to ETS will reduce the cardiomyocyte survival rate and accelerate age-related cardiac disease in aging animals [11, 22]. However, cell death and cell apoptosis can not be detected in the ETS exposure group comprising C57BL mice hearts (Figure 1).…”

Section: Discussionmentioning

confidence: 85%

“…The GYTS discovered that deaths that were caused by smoking were twice the number of those who started to smoke before the age of eighteen [8, 9, 10]. In our previous study, we discovered that ETS exposure accelerated age-related cardiac disease and reduced the IGF-1 growth signaling in aging rat hearts [11, 12]. Furthermore, ETS exposure can disturb the oxidative processes in myocardial mitochondria and lead to cardiomyopathy [13].…”

Section: Introductionmentioning

confidence: 99%

Environmental tobacco smoke increases autophagic effects but decreases longevity associated with Sirt-1 protein expression in young C57BL mice hearts

et al. 2016

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Recently, a survey by the Centers for Disease Control and Prevention (CDC) reported that nearly 90% of U.S. adult smokers began smoking at the age of 18. This demonstrates that the exposure to environmental tobacco smoke (ETS) of youngsters today is changing from passive smoking to active smoking (direct inhalation of tobacco). In the current study, an investigation of ETS exposure in young C57BL mice was conducted. After 6 weeks of ETS exposure, the Sirt-1 protein level was decreased and cardiac autophagy was increased in C57BL mice. Furthermore, the IGF2R cardiac hypertrophy signaling pathway was also triggered, although cardiac apoptosis and hypertrophy were not induced. Youngsters' desire to look more mature is one of the psychological factors that impacts smoking amongst young people. Our results suggest that though ETS exposure might cause cardiac autophagy amongst youngsters, the loss of the longevity Sirt-1 protein and the increase in IGF2R cardiac hypertrophy signaling could still promote heart diseases that are age-specific.

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Secondhand Smoke Exposure Reduced the Compensatory Effects of IGF-I Growth Signaling in the Aging Rat Hearts

Cited by 5 publications

References 34 publications

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

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

Effects of Cardiovascular Risk Factors on Cardiac STAT3

Environmental tobacco smoke increases autophagic effects but decreases longevity associated with Sirt-1 protein expression in young C57BL mice hearts

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