Role of endogenous negative regulators of STAT1 and STAT3 (SOCS-1, SOCS-3, PIAS1 and PIAS3) during experimental periodontal disease

• Grant number: 07/06658-7
• Support Opportunities: Regular Research Grants
• Start date: April 01, 2008
• End date: March 31, 2010
• Field of knowledge: Health Sciences - Dentistry - Periodontology
• Principal Investigator: Joni Augusto Cirelli
• Grantee: Joni Augusto Cirelli
• Host Institution: Faculdade de Odontologia (FOAr). Universidade Estadual Paulista (UNESP). Campus de Araraquara. Araraquara , SP, Brazil

Abstract

Inflammatory cytokine gene expression is a process strictly regulated by various mechanisms, including the negative regulation of signaling of cytokine receptors and of the activity of transcription factors such as STATs. These mechanisms involve endogenous proteins and is largely unknown, especially in periodontal diseases. Three groups of proteins, SHP, PIAS and SOCS modulate in a fairly specific manner JAK-STAT signaling and/or STAT activity. Periodontal diseases are infectious-inflammatory conditions of the supporting tissues of the teeth associated with increased levels of proinflammatory cytokines, but there are virtually no information regarding the role of these endogenous mediators of JAK-STAT during its course. The aims of this proposal include the study of the expression kinetics of inducible negative regulators, of their intracellular localization and of their physical interaction with their target proteins during the course of experimentally-induced periodontal disease. Using this model, we propose to evaluate the dynamics of expression, intracellular localization and physical interaction of SOCS-1, SOCS-3, PIAS1 and PIAS3 with STAT1 and STAT3 by means of real time RT-PCR, Western blotting and immunoprecipitation. Information derived from this proposal will contribute to the understanding of role of these endogenous negative regulators of JAK-STAT during inflammatory periodontal disease. (AU)

Scientific publications

(4)

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

CHAVES DE SOUZA, JOAO ANTONIO; BOAS NOGUEIRA, ANDRESSA VILAS; CHAVES DE SOUZA, PEDRO PAULO; KIM, YEON JUNG; LOBO, CAROLINE SILVA; PIMENTEL LOPES DE OLIVEIRA, GUILHERME JOSE; CIRELLI, JONI AUGUSTO; GARLET, GUSTAVO POMPERMAIER; ROSSA, CARLOS, JR.. SOCS3 Expression Correlates with Severity of Inflammation, Expression of Proinflammatory Cytokines, and Activation of STAT3 and p38 MAPK in LPS-Induced Inflammation In Vivo. Mediators of Inflammation, v. 2013, p. 10-pg., 2013-01-01. (07/06658-7, 07/06332-4)

CHAVES DE SOUZA, JOAO ANTONIO; BOAS NOGUEIRA, ANDRESSA VILAS; CHAVES DE SOUZA, PEDRO PAULO; KIM, YEON JUNG; LOBO, CAROLINE SILVA; PIMENTEL LOPES DE OLIVEIRA, GUILHERME JOSE; CIRELLI, JONI AUGUSTO; GARLET, GUSTAVO POMPERMAIER; ROSSA, JR., CARLOS. SOCS3 Expression Correlates with Severity of Inflammation, Expression of Proinflammatory Cytokines, and Activation of STAT3 and p38 MAPK in LPS-Induced Inflammation In Vivo. Mediators of Inflammation, 2013. (07/06332-4, 07/06658-7)

CHAVES DE SOUZA, JOAO ANTONIO; BOAS NOGUEIRA, ANDRESSA VILAS; CHAVES DE SOUZA, PEDRO PAULO; CIRELLI, JONI AUGUSTA; GARLET, GUSTAVO POMPERMAIER; ROSSA, JR., CARLOS. Expression of suppressor of cytokine signaling 1 and 3 in ligature-induced periodontitis in rats. ARCHIVES OF ORAL BIOLOGY, v. 56, n. 10, p. 1120-1128, OCT 2011. (07/06332-4, 07/06658-7)

CHAVES DE SOUZA, JOAO ANTONIO; ROSSA JUNIOR, CARLOS; GARLET, GUSTAVO POMPERMAIER; BOAS NOGUEIRA, ANDRESSA VILAS; CIRELLI, JONI AUGUSTO. Modulation of host cell signaling pathways as a therapeutic approach in periodontal disease. Journal of Applied Oral Science, v. 20, n. 2, p. 128-138, MAR-APR 2012. (07/06332-4, 07/06658-7)