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Investigation of the role of nitric oxide and RHO-GTPases in neutrophils adhesion, under inflammatory conditions

Grant number: 10/17138-7
Support type:Scholarships in Brazil - Master
Effective date (Start): March 01, 2011
Effective date (End): July 31, 2012
Field of knowledge:Biological Sciences - Pharmacology
Principal Investigator:Nicola Amanda Conran Zorzetto
Grantee:Angélica Aparecida Antoniellis Silveira
Home Institution: Centro de Hematologia e Hemoterapia (HEMOCENTRO). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil

Abstract

During the inflammatory response, neutrophils and other leukocytes adhere to the endothelium, before their extrasvasation from the blood vessel in the direction of the site of inflammation. The migration of the neutrophils depends on a series of adhesive and chemotactic events that result from receptor- mediated cell activation, involving interactions between selectins, integrins, and other adhesion molecules, and chemotactic receptors. Due to their phagocytic properties, the neutrophils can be activated by small intracellular signaling proteins, called the Rho GTPases, which mediate the neutrophil function by interfering in cytoskeleton alterations. These proteins are also involved in cell adhesion and proliferation. The neutrophils are able to synthesize nitric oxide (NO), and the production of this signaling molecule plays an important part in the inate immune response during infection. As such, this study aims to investigate the role of NO and Rho GTPase-dependent signaling pathways in the adhesive properies of neutrophils, under inflammatory conditions, using methods of static and flow adhesion (Venaflux Plataform) and flow cytometry. Results may provide further knowledge regarding the envolvement of NO and Rho GTPases in the inflammatory process. The understanding of these signaling pathways may be important for the identification of possible therapeutic targets for diseases whose pathophysiology is characterized by inflamation or chronic vascular inflammation.