| Grant number: | 15/16799-3 |
| Support type: | Regular Research Grants |
| Duration: | February 01, 2016 - January 31, 2018 |
| Field of knowledge: | Biological Sciences - Biochemistry - Molecular Biology |
| Principal researcher: | Edgar Julian Paredes-Gamero |
| Grantee: | Edgar Julian Paredes-Gamero |
| Home Institution: | Pró-Reitoria Acadêmica. Universidade de Mogi das Cruzes (UMC). Campus da Sede Mogi das Cruzes. Mogi das Cruzes , SP, Brazil |
| Assoc. researchers: | Alice Teixeira Ferreira |
Abstract
The intracellular Ca2+ is the most versatile second messenger. This ion participates in several cellular processes such as proliferation, differentiation, cell death, contraction, secretion, and even at fertilization and learning. These cellular processes are regulated by temporal, spatial and intensity variation of this ion. Our group has been studying the role of Ca2+ ion in the proliferation and differentiation of hematopoietic stem cell. So far we have determined that small increases of intracellular Ca2+ caused by cytokines are related to proliferation of HSC without decreasing their amount. On the other hand large increases of the intracellular Ca2+, caused by purinergic agonists, lead to differentiation of HSC. This effect has been observed in both murine and human HSC. However, a detailed description of Ca2+ ions events that modulate the proliferation and differentiation of HSC in their progeny, details such as location, signal strength and frequency is still needed. In addition, the Ca2+ signaling that leads to proliferation or differentiation is related with proteins which regulate hematopoiesis, and are sensitive to variations of calcium ion, however these proteins that have not yet been identified. Thus, in this project we want to better explore the intracellular Ca2+ signaling pathway by investigating important aspects of Ca2+ signaling such as spatial, temporal and intensity features and try to correlate them to the activation of signaling proteins that regulate hematopoiesis. Then, once identified the pattern of Ca2+ signaling in normal HSC, we want to compare this signal with the leukemic stem cells extracted from a murine leukemic lineage. (AU)