Fernanda Gallinaro Pessoa
University of São Paulo
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Featured researches published by Fernanda Gallinaro Pessoa.
PLOS ONE | 2017
A. M. de Oliveira-Fonoff; Charles Mady; Fernanda Gallinaro Pessoa; Keila C.B. Fonseca; Vera Maria Cury Salemi; Fábio Fernandes; Paulo Hilário Nascimento Saldiva; Felix José Alvarez Ramires; Qinghua Sun
Background Excessive air pollution in urban environments can impact morbidity and mortality. The authors evaluated the role of particulate matter2.5 (PM2.5) in structural, geometric, and functional remodeling in hearts, using an experimental model of myocardial infarction. Methods and findings Seventy-five rats were divided into 5 groups: control (CG), CG exposed to PM2.5 pollution (CGP), myocardial infarcted group (MI), infarcted group immediately exposed to pollution (IGP-I), and infarcted group previously exposed to pollution and kept exposed after infarction (IGP-II). Greater deposition of interstitial collagen occurred in the left ventricle in CGP, MI, IGP-I, and IGP-II groups compared with that in controls (p = 0.002 CG vs CGP and p<0.0001 CG vs MI, IGP-I, and IGP-II). In the right ventricle, greater collagen deposition existed in CGP, MI, IGP-I, and IGP-II compared with that in CG (p<0.021 CG vs CGP and p<0.0001 CG vs MI, IGP-I, and IGP-II). At the end of the study, CG had a higher mean shortening fraction than the other groups had (p≤0.03). Left ventricular systolic diameter was lower in CG than in infarcted groups (p≤0.003). The infarcted groups had greater expression of TGF-β (p≤0.04). PM2.5 increased the expression of TGF-β in the IGP-II compared with the MI group (p = 0.004). The TNF-α gene was overexpressed in the IGP-II compared with the CGP group (p = 0.012). INF-γ gene expression was greater in IGP-II (p≤0.01). Oxidative stress analysis showed a higher glutathione concentration in CGP (p = 0.03), MI (p = 0.014), and IGP-I (p = 0.008) compared with that in CG. Conclusions PM2.5 stimulates the deposition of fibrosis in the myocardium of healthy hearts, but not in infarcted hearts. PM2.5 modulates the inflammatory response, which was greater in the IGP-II group. It also modulates oxidative stress in healthy hearts but not in infarcted hearts.
Canadian Journal of Physiology and Pharmacology | 2018
Fernanda Gallinaro Pessoa; Prof.Dr. Charles Mady; Keila C.B. Fonseca; Adriana M. Oliveira-Fonoff; Prof.Dr. Vera M C Salemi; Mauricio R Jordao; Prof.Dr. Fabio Fernandes; Prof.Dr. Felix J A Ramires
Myocardial remodeling includes inappropriate collagen deposition in the interstitium. Erythropoietin (EPO) may have cardioprotective effects. We aimed to assess the role of EPO on myocardial remodeling during the chronic phase. We studied 60 Wistar rats divided into the following groups: control (CT), control + EPO (CT + EPO), myocardial infarction + EPO (MI + EPO), and myocardial infarction (MI). The interstitial collagen volume fraction (ICVF) was quantified and echocardiography was performed. We quantified asymmetric dimethylarginine and glutathione by ELISA, and used real-time PCR to assess apoptosis and inflammation. Western blotting was used to evaluate inflammatory proteins and tissue inhibitors of metalloproteinases (TIMPs), and TUNEL staining was used to detect apoptosis. For matrix metalloproteinases (MMPs), we performed zymography. Parametric and nonparametric analyses were performed according to normality testing. ICVF was greater in MI groups (p < 0.001) and was attenuated by EPO (p = 0.05). The MMP-2 did not show any difference between groups. The TIMP-1 and TIMP-2 did not have difference between groups. The MI groups had worse fraction shortening (p < 0.001), without EPO protection (p = 0.666). The MI groups had increased left ventricle diastolic dimension (p < 0.001) without EPO attenuation (p = 0.79). EPO did not act on oxidative stress. Apoptosis and inflammation were not modulated by EPO. We concluded that EPO attenuated interstitial collagen accumulation, but did not protect from heart dilation or dysfunction.
Journal of Cardiac Failure | 2012
Fábio Fernandes; Felix José Alvarez Ramires; Barbara Maria Ianni; Vera Maria Cury Salemi; Adriana Morgan Oliveira; Fernanda Gallinaro Pessoa; Mauro Canzian; Charles Mady
European Heart Journal | 2018
A S O Sarmento; L M Antunes-Correa; Maria Janieire N. N. Alves; A V N Bacurau; Keila C.B. Fonseca; Fernanda Gallinaro Pessoa; I C Trombetta; Maria Upb Rondon; Felix José Alvarez Ramires; M S Brasileiro-Santos; Patricia C. Brum; Charles Mady; Carlos Eduardo Negrão; S Thomas; Barbara Maria Ianni; Cardiomyopathies
Journal of the American College of Cardiology | 2017
Fernanda Gallinaro Pessoa; Keila C.B. Fonseca; Charles Mady; Orlando N. Ribeiro; Adriana M. Oliveira-Fonoff; Vera Maria Cury Salemi; Paulo Hilário Nascimento Saldiva; Fábio Fernandes; Felix José Alvarez Ramires
European Heart Journal | 2017
M.R. Jordao; F. Zanoni; Fernanda Gallinaro Pessoa; Keila C.B. Fonseca; Vera Maria Cury Salemi; L.E. Souza; O.N. Ribeiro; F. Fernandez; Charles Mady; Felix José Alvarez Ramires
Journal of Cardiac Failure | 2014
Adriana M.O. Fonoff; Felix José Alvarez Ramires; Keila C.B. Fonseca; Vera Maria Cury Salemi; Fernanda Gallinaro Pessoa; Paulo Hilário Nascimento Saldiva; Charles Mady
Archive | 2012
Abio Fernandes; Barbara Maria Ianni; Maria Cury Salemi; Adriana Morgan Oliveira; Fernanda Gallinaro Pessoa; Mauro Canzian; Charles Mady
Journal of the American College of Cardiology | 2012
Charles Mady; Leandro Tavares; Felix José Alvarez Ramires; Fernanda Gallinaro Pessoa; Adriana Morgan Oliveira; Júlio César Ayres Ferreira Filho; Fábio Fernandes; Vera Maria Cury Salemi
Journal of Cardiac Failure | 2012
Barbara Maria Ianni; Felix José Alvarez Ramires; Vera Maria Cury Salemi; Fábio Fernandes; Adriana Morgan Oliveira; Fernanda Gallinaro Pessoa; Keila C.B. Fonseca; Edmundo Arteaga; Luciano Nastari; Charles Mady