| Grant number: | 12/10435-1 |
| Support Opportunities: | Scholarships in Brazil - Post-Doctoral |
| Start date: | October 01, 2012 |
| End date: | April 30, 2017 |
| Field of knowledge: | Health Sciences - Medicine - Medical Clinics |
| Principal Investigator: | Niels Olsen Saraiva Câmara |
| Grantee: | Mariane Tami Amano |
| Host Institution: | Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil |
| Associated research grant: | 12/02270-2 - New cellular, molecular and immunological mechanisms involved in acute and chronic renal injury: the search for new therapeutical approaches, AP.TEM |
| Associated scholarship(s): | 14/20861-3 - The role of cohesin mutations in myeloid malignancies development, BE.EP.PD |
Abstract The mTOR signaling pathway can be activated by several molecules including insulin and IGF-1, besides it can also be activated after binding of immune system receptors as T cells (TCR), B cells (BCR) and toll-like receptors (TLR). There are two mTOR complexes, mTORC1 and mTORC2, that differ in crucial components of the signalization, as the presence of raptor and rictor respectively. Recently, it was demonstrated that Th1 and Th17 polarization required mTORC1 activation and the Th2 differentiation required mTORC2 activation. Taking into consideration that the macrophage differentiation to M1 depends on IFN-g and to M2 depends on IL-4 and IL-13, Th1 and Th2 cytokines respectively, we questioned whether M1/M2 polarization could depend on mTORC1 and/or mTORC2 activation. The macrophages subtypes differentiation seems to be fundamental in diseases physiopathogenis like chronic kidney disease. Then, we questioned whether M1/M2 polarization in this model could depend on mTORC1 and mTORC2 activation. Moreover, the macrophages subtypes differentiation seems to be fundamental to diseases physiopathogenia as chronic kidney disease (CKD). Thus, in this project, we aim to verify the role of mTOR complexes (mTORC1/2) in M1 and M2 macrophages polarization and verify the activation prevalence of these complexes in chroninc renal injury by inducing the unilateral ureteral obstruction (UUO). This study intend to investigate for the first time the role of mTORC1/2 in M1 and M2 modulation, and also in an unprecedented manner unveil the mechanisms of mTOR complexes in CKD development. | |
| News published in Agência FAPESP Newsletter about the scholarship: | |
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