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Unveiling the role of HSPB1 in prolactin-induced cytoprotection in pancreatic beta cells

Grant number: 14/17974-0
Support type:Scholarships in Brazil - Master
Effective date (Start): March 01, 2015
Effective date (End): December 31, 2015
Field of knowledge:Biological Sciences - Biochemistry - Molecular Biology
Cooperation agreement: Coordination of Improvement of Higher Education Personnel (CAPES)
Principal researcher:Leticia Labriola
Grantee:Vinícius de Morais Gomes
Home Institution: Instituto de Química (IQ). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

One of the goals in the treatment of type 1 diabetes is to enhance pancreatic beta-cell function, proliferation and survival. Beta-cell apoptosis occurs in diabetes where genes of the bcl-2 familyare known to either promote or to inhibit it. Results from our lab have shown significant prolactin-induced cytoprotection against apoptosis in beta-cells after the different cell death inducing conditions tested (serum starvation and cytokines treatment). In addition, we reported up-regulation of HSPB1, a member of the small heat shock proteins family presenting among others, chaperone function, upon rhPRL treatment. Even when members of the family of the heat shock proteins are known to mitigate apoptosis after numerous challenges, the cytoprotective effects of HSPB1 on beta-cells have not been directly studied. Unpublished results from our lab have shown that prolactin cytoprotection is, at least partially, mediated byHSPB1. The accumulation of unfolded proteins cause Endoplasmic Reticulum Stress (ERstress) which can trigger different cell fates. Indeed, results from Dr. Décio Eizirik and Dr.Alessandra Cardozo's group at the Université Libre de Bruxelles, have already shown acorrelation between cytokines, involved in the development of DM1, and endoplasmic reticulum stress induction. Until today, there is no data relating HSPB1, a small ATP independent chaperone, to attenuation of beta-cell ER-stress. Therefore, in this work we set out to study whether HSPB1 could also act as a mediator of beta-cell rhPRL-induced cytoprotection in response to ER stress. The ultimate goal of this project is to increase the quality of beta-cells available for transplantation and so, our results could lead to the development of novel method of is let cytoprotection based on this approach. (AU)

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.; 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; LABRIOLA, LETICIA. 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. Web of Science Citations: 0.
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. Web of Science Citations: 1.

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