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Defining the impact of E-Cigarettes on cardiac pathophysiology

Grant number: 18/15461-7
Support Opportunities:Scholarships abroad - Research Internship - Doctorate
Effective date (Start): October 31, 2018
Effective date (End): October 30, 2019
Field of knowledge:Health Sciences - Physical Education
Principal Investigator:Leandro Pereira de Moura
Grantee:Chadi Pellegrini Anaruma
Supervisor: Loren E. Wold
Host Institution: Instituto de Biociências (IB). Universidade Estadual Paulista (UNESP). Campus de Rio Claro. Rio Claro , SP, Brazil
Research place: Ohio State University, Columbus, United States  
Associated to the scholarship:16/14388-9 - Comparison of two exercise protocols on action mechanism of clusterin/ApoJ in lean and obese mice, BP.DR


Both cigarettes and air pollution are sources of toxic gases and fine particulate matter (PM2.5; particles <2.5 µm) that are linked with adverse CV outcomes, characterized by increased inflammation and subsequent collagen deposition. Recently, a new source of emissions, the electronic cigarette (EC), was introduced and is gaining unprecedented popularity, especially among young people. Although e-cigarettes are an artificial source of nicotine similar to tobacco cigarettes, they are a source of potentially toxic gases, fine particulates, and nicotine. However, it remains unknown if e-cigarette use increases inflammation and fibrosis long-term, leading to structural and functional damage to heart and vasculature; these critical questions will be answered by the present proposal using in vivo models and, for the first time, primary human myocytes. Aerosol from ECs are comprised of fine and ultrafine particles which makes it relevant to investigate plausible effects of EC exposure on inflammatory and calcium regulatory pathway. Studies from our team demonstrate that exposure to fine particulate matter cause long-term cardiac dysfunction. In fact, our data are the first to examine the adverse CV consequences of exposure to PM 2.5, and will be expanded to include similar studies on EC generated aerosol. While our findings in mice support the critical impact of EC aerosol in mice, given the growing population already exposed to EC aerosols, it is critical that we now translate our studies to define the impact on key surrogate cardiac cell populations. We have established a live cell repository of key cardiac cell populations from non-failing and diseased human heart. We will take advantage of this now well validated resource to perform parallel functional experiments in both mice and human. We hypothesize that EC aerosol promotes both acute and chronic damage to multiple cardiac cell populations resulting in severe organ and organism dysfunction. The goals of this investigation are to define the impact of EC aerosol (in clinically relevant concentrations) on animals and well phenotyped human cardiac myocytes. We will 1) define the in vivo impact of acute and chronic EC aerosol exposure on cardiac physiology, 2) define the impact of acute and chronic EC aerosol exposure on the function of key cardiac cell populations, and 3), Define the impact of EC aerosol exposure on key primary human cardiac cell populations. (AU)

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Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
ANARUMA, CHADI PELLEGRINI; PEREIRA, RODRIGO MARTINS; DA CRUZ RODRIGUES, KELLEN CRISTINA; RAMOS DA SILVA, ADELINO SANCHEZ; CINTRA, DENNYS ESPER; ROPELLE, EDUARDO ROCHETE; PAULI, JOSE RODRIGO; DE MOURA, LEANDRO PEREIRA. Rock protein as cardiac hypertrophy modulator in obesity and physical exercise. Life Sciences, v. 254, . (18/15461-7, 16/14388-9, 15/07199-2)

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