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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

SOCS3 Expression Correlates with Severity of Inflammation, Expression of Proinflammatory Cytokines, and Activation of STAT3 and p38 MAPK in LPS-Induced Inflammation In Vivo

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Chaves de Souza, Joao Antonio [1] ; Boas Nogueira, Andressa Vilas [1] ; Chaves de Souza, Pedro Paulo [2] ; Kim, Yeon Jung [3] ; Lobo, Caroline Silva [1] ; Pimentel Lopes de Oliveira, Guilherme Jose [1] ; Cirelli, Joni Augusto [1] ; Garlet, Gustavo Pompermaier [4] ; Rossa, Jr., Carlos [1]
Total Authors: 9
[1] Univ Estadual Paulista UNESP, Sch Dent Araraquara, Dept Diag & Surg, BR-14801903 Araraquara, SP - Brazil
[2] Univ Estadual Paulista UNESP, Dept Physiol & Pathol, Sch Dent Araraquara, BR-14801903 Araraquara, SP - Brazil
[3] Univ Santo Amaro, Dept Implantol, BR-04743030 Santo Amaro, SP - Brazil
[4] Univ Sao Paulo, Sch Dent Bauru, Dept Biol Sci, BR-17012901 Bauru, SP - Brazil
Total Affiliations: 4
Document type: Journal article
Source: Mediators of Inflammation; 2013.
Web of Science Citations: 25

SOCS3 is an inducible endogenous negative regulator of JAK/STAT pathway, which is relevant in inflammatory conditions. We used a model of LPS-induced periodontal disease in rats to correlate SOCS3 expression with the inflammatory status. In vitro we used a murine macrophage cell line to assess the physical interaction between SOCS3 and STAT3 by coimmunoprecipitation. 30 ug of LPS from Escherichia coli were injected in the gingival tissues on the palatal aspect of first molars of the animals 3x/week for up to 4weeks. Control animals were injected with the vehicle (PBS). The rats were sacrificed at 7, 15, and 30 days. Inflammation and gene expression were assessed by stereometric analysis, immunohistochemistry, RT-qPCR, and western blot. LPS injections increased inflammation, paralleled by an upregulation of SOCS3, of the proinflammatory cytokines IL-beta, IL-6, and TNF-alpha and increased phosphorylation of STAT3 and p38 MAPK. SOCS3 expression accompanied the severity of inflammation and the expression of proinflammatory cytokines, as well as the activation status of STAT3 and p38 MAPK. LPS stimulation in a macrophage cell line in vitro induced transient STAT3 activation, which was inversely correlated with a dynamic physical interaction with SOCS3, suggesting that this may be a mechanism for SOCS3 regulatory function. (AU)

FAPESP's process: 07/06658-7 - Role of endogenous negative regulators of STAT1 and STAT3 (SOCS-1, SOCS-3, PIAS1 and PIAS3) during experimental periodontal disease
Grantee:Joni Augusto Cirelli
Support type: Regular Research Grants
FAPESP's process: 07/06332-4 - Role of endogenous negative regulators of STAT1 and STAT3 (SOCS-1, SOCS-3, PIAS1 and PIAS3) during experimental periodontal disease
Grantee:João Antonio Chaves de Souza
Support type: Scholarships in Brazil - Master