2010
DOI: 10.1074/jbc.m110.132084
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Suppressor of Cytokine Signaling 3 Inhibits LPS-induced IL-6 Expression in Osteoblasts by Suppressing CCAAT/Enhancer-binding Protein β Activity

Abstract: Suppressor of cytokine signaling 3 (SOCS3) is an important intracellular protein that inhibits cytokine signaling in numerous cell types and has been implicated in several inflammatory diseases. However, the expression and function of SOCS3 in osteoblasts are not known. In this study, we demonstrated that SOCS3 expression was transiently induced by LPS in osteoblasts, and apparently contributed to the inhibition of IL-6 induction by LPS treatment. We found that tyrosine 204 of the SOCS box, the SH2 domain, and… Show more

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Cited by 39 publications
(44 citation statements)
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“…Injections of Escherichia coli LPS in the palatal gingival tissues of first 645332J DRXXX10.1177/0022034516645332Journal of Dental ResearchSOCS-3 Regulates Alveolar Bone Loss research-article2016 molars of rats increased inflammation; induced an upregulation of SOCS-3 expression paralleled by an increase of the proinflammatory cytokines IL-1β, IL-6, and TNF-α; and increased phosphorylation of STAT3 (Chaves de Souza et al 2013). SOCS-3 downregulates additional proinflammatory mediators induced by LPS in osteoblasts, thereby playing a critical role in osteoblast-mediated immune signaling (Yan et al 2010;Gao et al 2013). The analysis of mice lacking genes for SOCS proteins has shed additional light on their critical importance in restraining inflammation and allowing optimal levels of protective immune responses in several inflammatory disorders, including arthritis, atherosclerosis, and cancer (Wong et al 2006;Recio et al 2015;Yu et al 2015).…”
Section: Introductionmentioning
confidence: 99%
“…Injections of Escherichia coli LPS in the palatal gingival tissues of first 645332J DRXXX10.1177/0022034516645332Journal of Dental ResearchSOCS-3 Regulates Alveolar Bone Loss research-article2016 molars of rats increased inflammation; induced an upregulation of SOCS-3 expression paralleled by an increase of the proinflammatory cytokines IL-1β, IL-6, and TNF-α; and increased phosphorylation of STAT3 (Chaves de Souza et al 2013). SOCS-3 downregulates additional proinflammatory mediators induced by LPS in osteoblasts, thereby playing a critical role in osteoblast-mediated immune signaling (Yan et al 2010;Gao et al 2013). The analysis of mice lacking genes for SOCS proteins has shed additional light on their critical importance in restraining inflammation and allowing optimal levels of protective immune responses in several inflammatory disorders, including arthritis, atherosclerosis, and cancer (Wong et al 2006;Recio et al 2015;Yu et al 2015).…”
Section: Introductionmentioning
confidence: 99%
“…A variety of cells express SOCS3, including macrophages, osteoblasts, microglia, and neutrophils [4, 18, 24], and roles of SOCS3 in inflammation have been investigated. However, the effect of SOCS3 on inflammatory responses after FcγR cross-linking remains largely unknown.…”
Section: Resultsmentioning
confidence: 99%
“…Besides STAT3, SOCS3 could also repress inflammatory responses through other mechanisms. Our recent studies have proved that SOCS3 decreases IL-6 expression in osteoblasts incubated with LPS by inhibiting C/EBPβ DNA binding activity [4]. In contrast to the above reports, SOCS3 could also act as an inflammatory promoter.…”
Section: Introductionmentioning
confidence: 99%
“…We speculated that while VDR primarily regulates inflammatory responses by suppressing NF-κB activity, VDR deletion may induce compensatory immunoregulatory mechanisms in the intestine. Since suppressor of cytokine signaling (SOCS) 1 and SOCS3 have been reported to inhibit LPS-induced IL-6 production [48], [49], we examined the expression of Socs1 and Socs3 in the intestine. There was no difference in Socs1 expression in sham-operated wild-type, BDL wild-type, sham-operated VDR-null and BDL VDR-null mice, although BDL tended to decrease Socs1 expression in wild-type mice (Fig.…”
Section: Resultsmentioning
confidence: 99%