Interleukin-1: The principal osteolytic cytokine produced by keratocysts

Meghji, S; Henderson, Brian E.; Bando, Yasuhiro; Harris, Malcolm

doi:10.1016/0003-9969(92)90065-g

Cited by 41 publications

(34 citation statements)

References 24 publications

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“…Indomethacin has been reported to suppress IL-1-induced osteoclast formation dramatically (Chen et al, 1997;Tai et al, 1997), suggesting a pathological importance for PGE 2 in osteoclastogenesis by IL-1. IL-1␣ has been reportedly expressed in the subepithelial fibroblasts as well as the epithelial cells in odontogenic keratocysts (Meghji et al, 1992;Ninomiya et al, 2002). The present study showed that COX-2 was expressed in the subepithelial layer fibroblasts of odontogenic keratocysts.…”

Section: Discussionsupporting

confidence: 59%

Signaling Pathways Regulating IL-1α-induced COX-2 Expression

et al. 2007

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Interleukin-1alpha(IL-1alpha) stimulates the production of prostaglandin E(2) (PGE(2)) in odontogenic keratocyst fibroblasts. However, the signaling pathways remain obscure. In this study, we investigated IL-1alphasignaling pathways that regulate cyclooxygenase-2 (COX-2) expression in odontogenic keratocyst fibroblasts. IL-1alphaincreased the expression of COX-2 mRNA and protein, and PGE(2) secretion in the fibroblasts. IL-1alphaincreased the phosphorylation of extracellular signal-regulated protein kinase-1/2 (ERK1/2), p38 mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK). PD-98059, SB-203580, SP-600125, and PDTC-which are inhibitors of ERK1/2, p38, JNK, and nuclear factor-kappaB (NF-kappaB), respectively-attenuated the IL-1alpha-induced COX-2 mRNA expression and activated protein kinase C PGE(2) secretion. IL-1alpha(PKC), and PKC inhibitor staurosporine inhibited IL-1alpha-induced phosphorylation of ERK1/2, p38, and JNK, and decreased IL-1alpha-induced COX-2 mRNA expression. Thus, in odontogenic keratocyst fibroblasts, IL-1alphamay stimulate COX-2 expression both through the PKC-dependent activation of ERK1/2, p38, and JNK signaling pathways, and through the NF-kappaB cascade.

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Section: Discussionsupporting

confidence: 59%

Signaling Pathways Regulating IL-1α-induced COX-2 Expression

et al. 2007

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“…Type I collagen is widely expressed not only in bone but also in the fibroblasts of the subepithelial layers of odontogenic keratocysts (unpublished observation). IL-1␣ is also expressed in the epithelial cells and the subepithelial fibroblasts of odontogenic keratocysts (Meghji et al, 1992(Meghji et al, , 1996Kubota et al, 2001). IL-1␣ is not degraded by MMP-1, -2, -3, or -9 (Ito et al, 1996).…”

Section: Discussionmentioning

confidence: 98%

“…Interleukin-1␣ (IL-1␣) is expressed in a lining epithelium, and fibroblasts and endothelial cells in the subepithelial layers of odontogenic keratocysts (Meghji et al, 1992(Meghji et al, , 1996Kubota et al, 2001). Recently, we have shown that IL-1␣ increases the activation of proMMP-2 in odontogenic jaw cyst fragments in explant culture (Kubota et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Interleukin-1 Enhances Type I Collagen-induced Activation of Matrix Metalloproteinase-2 in Odontogenic Keratocyst Fibroblasts

Kubota¹,

Oka²,

Nakagawa³

et al. 2002

Journal of Dental Research

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Interleukin-1alpha (IL-1alpha) is strongly expressed in odontogenic keratocysts. In this study, we investigated the effects of IL-1alpha on the activation of matrix metalloproteinase-2 (MMP-2) in the fibroblasts isolated from odontogenic keratocysts. Odontogenic keratocyst fibroblasts secreted a latent form of MMP-2 (proMMP-2) spontaneously. Type I collagen induced the activation of the proMMP-2, and recombinant human IL-1alpha (rhIL-1alpha) further enhanced the type I collagen-induced activation of proMMP-2 in a dose-dependent manner. The rhIL-1alpha-induced activation of proMMP-2 was inhibited by anti-human IL-1alpha antibody. A reverse-transcription/polymerase chain-reaction (RT-PCR) and Western immunoblotting demonstrated that the expression of membrane-type 1 matrix metalloproteinase (MT1-MMP) mRNA and protein was increased in the fibroblasts when the cells were cultured on type I collagen, and the expression was further enhanced by rhIL-1alpha. Thus, IL-1alpha may up-regulate proMMP-2 activation by increasing the expression of MT1-MMP in the fibroblasts isolated from odontogenic keratocysts synergistically with type I collagen.

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“…It has been shown that KCOTs express p53 suggesting their neoplastic nature. 31 Proliferating cell nuclear antigen (PCNA) is a marker of cell replication and is also associated with DNA repair process and stimulation by growth factors. A strong positivity was observed in KCOTs compared with dentigerous cysts and radicular cysts.…”

Section: Geneticsmentioning

confidence: 99%

Keratocystic Odontogenic Tumor of the Maxilla: Report of a Rare Case and Review of Literature

Nagaraja¹,

Anigol²,

Kamath³

et al. 2012

World Journal of Dentistry

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The odontogenic keratocyst (OKC) has recently been reclassified by the WHO (2005), as keratocystic odontogenic tumor (KCOT) based on clinical, histological and immunohistochemical parameters. KCOT more commonly occurs in the mandible and cases involving the maxilla are infrequent. We report an unusual and rare case of a KCOT of the maxilla in a middle-aged individual with extensive involvement and displacement of the maxillary third molar to the zygomatic region. A discussion of the parameters involved in the reclassification of the lesion as a tumor is presented alongwith a review of literature.

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Interleukin-1: The principal osteolytic cytokine produced by keratocysts

Cited by 41 publications

References 24 publications

Signaling Pathways Regulating IL-1α-induced COX-2 Expression

Signaling Pathways Regulating IL-1α-induced COX-2 Expression

Interleukin-1 Enhances Type I Collagen-induced Activation of Matrix Metalloproteinase-2 in Odontogenic Keratocyst Fibroblasts

Keratocystic Odontogenic Tumor of the Maxilla: Report of a Rare Case and Review of Literature

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