Claudia González Espinosa, PhD
Laboratory of Inflammation and Signal Transduction in Mast Cells
Position: Titular Researcher Cinvestav 3D, SNI III.
PhD: Basic Biomedical Research, National Autonomous University of Mexico,1995.
MSc: Basic Biomedical Research, National Autonomous University of Mexico,1992.
Bsc: Basic Biomedical Research, National Autonomous University of Mexico,1989.
Molecular Inflammation Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health, Bethesda, Maryland, USA, 199-2001.
Cell Biology Department, Cell Physiology Institute, Nat. Aut. Univ. Mex. (UNAM), 1996-1998
Signal Transduction Systems involved in the control of synthesis and secretion of pro-inflammatory and pro-angiogenic mediators in mast cells.
Molecular mechanisms of inflammation associated to allergic reactions, Neuroinflammation and tumor growth.
Participation of mast cells in distinct innate and adaptive immune responses and tumor angiogénesis and their control by novel multitarget and specific drugs.
Neuroendocrine control of mast cell-dependent immune reactions.
- To establish the relationship between stimulus-intensity and specific cytokine synthesis after triggering of the high affinity IgE receptor (FceRI) in mast cells.
- To describe several molecular mechanisms involved in pro-angiogenic activity of mast cells in solid tumors, like the presence of monomeric IgE, hypoxia and glutationylation of L-type L calcium channels.
- To find that pro-inflammatory innate immunity reactions mediated by mast cells are negatively regulated by the anti-inflammatory cholinergic réflex, opioids and endocannabinoids.
- To describe the participation of protein Huntingtin (whose mutation causes Huntington Disease) in cytokine production induced by innate immunity stimuli in mast cells.
Selected recent publications:
1. Signal transduction pathways activated by innate immunity in mast cells: translating sensing of changes into specific responses. Espinosa-Riquer, Z.P., Segura-Villalobos, D., Ramírez-Moreno, Itzel G. Pérez-Rodríguez, M. J., Lamas, M., González-Espinosa, C. Cells 9: 2411, 2020. doi: 10.3390/cells9112411
2. Mutant Huntingtin affects Toll-like receptor 4 intracellular trafficking and cytokine production in mast cells. Pérez-Rodríguez, M.J., Ibarra-Sánchez, A., Román-Figueroa, A., Pérez-Severiano, F., and González-Espinosa, C. Journal of Neuroinflammation, 17:95, 2020. doi.org/10.1186/s12974-020-01758-9
3. Mast cells localize in hypoxic zones of tumors and secrete CCL-2 under hypoxia through activation of L-type calcium channels. Ramírez-Moreno, I.G., Ibarra-Sánchez, A., Castillo-Arellano, J.I., Blank, U., and González-Espinosa, C. The Journal of Immunology, 204(4): 1056-1068, 2020. pii: ji1801430. doi: 10.4049/jimmunol.1801430.
4. TLR4 receptor induces 2-AG-dependent tolerance to Lipopolysaccharide and trafficking of CB2 receptor in mast cells. Espinosa-Riquer, Z., Ibarra-Sánchez, A., Vibhushan, S., Bratti, M., Charles, N., Blank, U., Rodríguez-Manzo, G., González-Espinosa, C. The Journal of Immunology, 202 (8):2360-2371, 2019. doi: 10.4049/jimmunol.1800997
Main current projects:
- Characterization of phenotypic changes caused by cyclic hypoxia found in tumor microenvironment in mast cells.
- Characterization of the molecular mechanisms involved in the inhibition of mast cell activity by G-protein-coupled receptors.
- Participation of innate immunity receptors on the recruitment of mast cells to solid tumors and cytokine production in tumor microenvironment.
- Pharmacologic control of allergic reactions utilizing natural products and multitarget compounds combined with specific molecules, using in vitro and in vivo models.
- Elucidation of the participation of mast cells, and their specific receptors and products in preclinical models of Neuroinflammation.