Autophagy in beta-cells and the cytoprotective roles of prolactin

• Grant number: 13/13914-0
• Support Opportunities: Scholarships in Brazil - Post-Doctoral
• Start date: December 01, 2013
• End date: June 30, 2017
• Field of knowledge: Biological Sciences - Biochemistry
• Principal Investigator: Leticia Labriola
• Grantee: Letícia Ferreira Terra
• Host Institution: Instituto de Química (IQ). Universidade de São Paulo (USP). São Paulo , SP, Brazil
• Associated scholarship(s): 16/02881-2 - PRL and HSPB1 effects in the autophagy and oxidative stress of beta-cells, BE.EP.PD

Abstract

Autophagy is a conserved physiological system of intracellular degradation, it can be considered as a cytoprotective mechanism; however, autophagy is also able to promote cell death by an altered degradation of cell content. Besides its physiological effect, it has been proposed that deregulation of this process may have important roles in several diseases; its role in diabetes is still obscure, but recent observations suggest that autophagy may have important roles in the development and prevention of diabetes. Unpublished results from our group in collaboration with Dr. Alessandra Cardozo's group at the Université Libre de Bruxelles, show a correlation between cytokines, known to have an important action in the development of DM1, and endoplasmic reticulum stressors, with autophagy induction in beta- cells. Results from our lab show that the addition of prolactin promotes significant cytoprotection against apoptosis in beta-cells after the different cell death-inducing conditions tested (serum starvation and cytokines treatment). In order to further analyze the cytoprotective capacity of PRL after other cell death-inducing mechanisms, we set out to investigate whether cotreatment with the hormone would lead to a restauration of the expression of autophagy markers after different combinations of cytokines and ER stressors, as well as after serum starvation. Collectively, our project aims at contribuiting to the mitigation of beta-cell death through the up-regulation of an endogenous protective pathway which is independent on the modulation of the immune system.

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)

TERRA, LETICIA F.; LOBBA, ALINE R. M.. High-fat diet and fish oil affect adipocyte metabolism in a depot-specific manner. JOURNAL OF PHYSIOLOGY-LONDON, v. 595, n. 6, p. 2-pg., 2017-03-15. (13/13914-0, 16/02881-2)

WAILEMANN, ROSANGELA A. M.; TERRA, LETICIA F.; OLIVEIRA, TALITA C.; DOS SANTOS, ANCELY F.; GOMES, VINICIUS M.; LABRIOLA, LETICIA. Heat shock protein B1 is required for the prolactin-induced cytoprotective effects on pancreatic islets. Molecular and Cellular Endocrinology, v. 477, p. 39-47, DEC 5 2018. (14/17974-0, 14/02745-6, 13/13914-0, 13/07029-4, 16/04676-7, 17/03618-6)

TERRA, LETICIA F.; WAILEMANN, ROSANGELA A. M.; DOS SANTOS, ANCELY F.; GOMES, VINICIUS M.; SILVA, RAILMARA P.; LAPORTE, ANNA; MEOTTI, FLAVIA C.; TERRA, WALTER R.; PALMISANO, GIUSEPPE; LORTZ, STEPHAN; et al. Heat shock protein B1 is a key mediator of prolactin-induced beta-cell cytoprotection against oxidative stress. Free Radical Biology and Medicine, v. 134, p. 394-405, APR 2019. (16/02881-2, 14/17974-0, 13/07029-4, 17/03618-6, 14/02745-6, 13/13914-0)