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Identification of neuroprotective myokines released by human skeletal muscle at low and high intensity contractions: role of mitochondrial bioenergetics and oxidative stress

Grant number: 16/23509-4
Support type:Regular Research Grants
Duration: February 01, 2017 - July 31, 2019
Field of knowledge:Biological Sciences - Biochemistry
Principal Investigator:Luciane Carla Alberici
Grantee:Luciane Carla Alberici
Home Institution: Faculdade de Ciências Farmacêuticas de Ribeirão Preto (FCFRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Assoc. researchers:Adriano Silva Sebollela ; Maria José Alves da Rocha

Abstract

Considering the rising aging of the population, studies on prevention/treatment of neurodegenerative diseases are actually of great importance; these diseases promote a high negative impact on the quality of life and on the economy. Clinically characterized by progressive loss of memory, cognitive impairment, and changes in social/occupational function, Alzheimer's disease (AD) leads to dementia, and eventually to death. AD not related to genetic inheritance is the most frequent; sedentary lifestyle, high body mass index, hypertension and diabetes mellitus are risk factors to AD. Studies in humans have suggested that physical activity is associated with reduced risk of developing neurodegenerative diseases, such as AD. However, the molecular mechanisms induced by physical exercise are not yet known. Then, the aims of present project are to evaluate: 1) myokines released by human skeletal muscle, in different intensities of exercise, whose present a neuroprotective effect against toxicity associated to DA; 2) if these myokines stimulate mechanisms of beta-amyloid oligomer clearance; 3) if aspects related to mitochondrial bioenergetics, oxidative and endoplasmic reticulum stresses are associated with myokine release; 4) whether mitochondrial changes induced in exercised skeletal muscle are also induced in neuronal cells (a potential crosstalking mitochondria-mitochondria). Cellular models (myotubes and neurons) and transgenic mice for AD, exercised in running will be used. As not all individuals can exercise because circumstances of disease or senescence-related fragility, the identification of peripheral factors and mechanisms that promote the effects of exercise on the brain can lead to therapies that protect against the development of AD. (AU)

Scientific publications (9)
(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)
SILVA, CAIO MATEUS; FERRARI, GUSTAVO DUARTE; ALBERICI, LUCIANE CARLA; MALASPINA, OSMAR; MORAES, KAREN C. M. Cellular and molecular effects of silymarin on the transdifferentiation processes of LX-2 cells and its connection with lipid metabolism. Molecular and Cellular Biochemistry, v. 468, n. 1-2 MAR 2020. Web of Science Citations: 0.
VULCZAK, ANDERSON; SOUZA, ANDERSON DE OLIVEIRA; FERRARI, GUSTAVO DUARTE; CALEIRO SEIXAS AZZOLINI, ANA ELISA; PEREIRA-DA-SILVA, GABRIELA; ALBERICI, LUCIANE CARLA. Moderate Exercise Modulates Tumor Metabolism of Triple-Negative Breast Cancer. CELLS, v. 9, n. 3 MAR 2020. Web of Science Citations: 0.
ROCHA CATALAO, CARLOS HENRIQUE; SOUZA, ANDERSON OLIVEIRA; SANTOS-JUNIOR, NILTON NASCIMENTO; DA SILVA, STEPHANYA COVAS; ANGENENDT DA COSTA, LUIS HENRIQUE; ALBERICI, LUCIANE CARLA; ALVES ROCHA, MARIA JOSE; LOPES, LUIZA DA SILVA. Kaolin-induced hydrocephalus causes acetylcholinesterase activity dysfunction following hypothalamic damage in infant rats. Brain Research, v. 1724, DEC 1 2019. Web of Science Citations: 0.
PORTO DECHANDT, CARLOS ROBERTO; FERRARI, GUSTAVO DUARTE; DOS SANTOS, JONATHAS RODRIGO; CORTES DE OLIVEIRA, JOSE ANTONIO; PATRICIO SILVA-JR, RUI MILTON; SIQUEIRA CUNHA, ALEXANDRA OLIMPIO; GARCIA-CAIRASCO, NORBERTO; ALBERICI, LUCIANE CARLA. Energy Metabolism and Redox State in Brains of Wistar Audiogenic Rats, a Genetic Model of Epilepsy. FRONTIERS IN NEUROLOGY, v. 10, OCT 1 2019. Web of Science Citations: 0.
AZEVEDO, LARA FERREIRA; PORTO DECHANDT, CARLOS ROBERTO; DE SOUZA ROCHA, CECILIA CRISTINA; HORNOS CARNEIRO, MARIA FERNANDA; ALBERICI, LUCIANE CARLA; BARBOSA JR, FERNANDO. Long-term exposure to bisphenol A or S promotes glucose intolerance and changes hepatic mitochondrial metabolism in male Wistar rats. Food and Chemical Toxicology, v. 132, OCT 2019. Web of Science Citations: 0.
PORTO DECHANDT, CARLOS ROBERTO; VICENTINI, TATIANE M.; LANFREDI, GUILHERME PAUPERIO; SILVA-JR, RUI M. P.; ESPREAFICO, ENILZA MARIA; CORTES DE OLIVEIRA, JOSE A.; FACA, VITOR MARCEL; GARCIA-CAIRASCO, NORBERTO; ALBERICI, LUCIANE CARLA. The highly efficient powerhouse in the Wistar audiogenic rat, an epileptic rat strain. AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, v. 316, n. 3, p. R243-R254, MAR 2019. Web of Science Citations: 1.
VICENTINI, TATIANE M.; CAVALHEIRO, AMANDA H.; DECHANDT, CARLOS R. P.; ALBERICI, LUCIANE C.; VARGAS-RECHIA, CAREM G. Aluminum directly inhibits alternative oxidase pathway and changes metabolic and redox parameters on Jatropha curcas cell culture. Plant Physiology and Biochemistry, v. 136, p. 92-97, MAR 2019. Web of Science Citations: 0.
SOUZA, ANDERSON DE OLIVEIRA; COUTO-LIMA, CARLOS ANTONIO; ROCHA CATALAO, CARLOS HENRIQUE; SANTOS-JUNIOR, NILTON NASCIMENTO; DOS SANTOS, JULIA FERNANDA; ALVES DA ROCHA, MARIA JOSE; ALBERICI, LUCIANE CARLA. Neuroprotective action of Eicosapentaenoic (EPA) and Docosahexaenoic (DHA) acids on Paraquat intoxication in Drosophila melanogaster. NeuroToxicology, v. 70, p. 154-160, JAN 2019. Web of Science Citations: 1.
CERVONI, MARIO S.; CARDOSO-JUNIOR, CARLOS A. M.; CRAVEIRO, GIOVANA; SOUZA, ANDERSON DE O.; ALBERICI, LUCIANE C.; HARTFELDER, KLAUS. Mitochondrial capacity, oxidative damage and hypoxia gene expression are associated with age-related division of labor in honey bee (Apis mellifera L.) workers. Journal of Experimental Biology, v. 220, n. 21, p. 4035-4046, NOV 1 2017. Web of Science Citations: 6.

Please report errors in scientific publications list by writing to: cdi@fapesp.br.