| Grant number: | 14/13052-1 |
| Support Opportunities: | Scholarships in Brazil - Post-Doctoral |
| Start date: | October 01, 2014 |
| End date: | December 31, 2017 |
| Field of knowledge: | Biological Sciences - Morphology - Cytology and Cell Biology |
| Principal Investigator: | Estela Maris Andrade Forell Bevilacqua |
| Grantee: | Aline Rodrigues Lorenzon |
| Host Institution: | Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil |
| Associated scholarship(s): | 17/06824-6 - Expression of Sdf2 in human placenta from preeclamptic and gestational diabetic patients, BE.EP.PD |
Abstract The Endoplasmic Reticulum (ER) is responsible for synthesis and addressing of secreted and membrane proteins. Adverse environmental conditions may lead to disruption of ER homeostasis causing accumulation of unfolded/misfolded proteins in ER, a phenomenon known as ER stress. ER stress activates the Unfolded Protein Response (UPR) that acts in several signaling cascades to improve chaperone production, misfolded protein degradation and to downregulate new protein production. These responses increase the capacity of cells to maintain alive even in stress conditions. Whether cells fail on restore homeostasis, the UPR activates apoptosis. The mechanisms that controls the switch between pro-survival to pro-apoptosis response is still unknown in UPR. The stromal cell derived factor 2 (SDF2) was first described by Hamada et al.(1996), is well conserved in mammals but its function is still unknown. In human and mouse, SDF2 has a paralogous gene, SDF2L1 (78% similar in protein sequence). Human SDF2L1 is an endoplasmic reticulum-stress inducible-gene, whose function is related to quality control of new synthesized proteins. In Arabidopsis thaliana, SDF2-like (39% sequence identity) has also been implicated in quality control and activation of UPR in ER-stress. Although the similarities of aminoacid predicted sequences of SDF2, its expression and function is still unknown. In your PhD project, the candidate was able to verify the participation of SDF2 in ER stress in placental cells (human and mouse, trophoblast cells). When gene silencing assays was used for SDF2, we were able to detected modifications in UPR cell survival/apoptosis markers. Therefore, in this project we propose to investigate the role played by SDF2 in ER stress cell survival/apoptosis control in trophoblast cells. | |
| News published in Agência FAPESP Newsletter about the scholarship: | |
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