Proinflammatory Cytokine Expression in Cyclooxygenase-2–deficient Primary Osteoblasts

He, Jianing; Tomlinson, Rosamond; Coon, David; Gulati, Ajay; Cowan, Cameron

doi:10.1016/j.joen.2007.08.001

Cited by 5 publications

(1 citation statement)

References 31 publications

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“…2). Interleukin-1β (IL-1β) and TNF-α stimulate the PGE 2 production of mouse osteoblasts (17). In addition, BisGMA, resin monomer released from composite resin, induces PGE 2 production in dental pulp cells (18).…”

Section: Discussionmentioning

confidence: 99%

Tannin-fluoride preparation attenuates prostaglandin E2 production by dental pulp cells

et al. 2011

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Abstract. Glass ionomer cements (GICs) are widely used for the operative restoration of dental caries. However, it has been reported that the components of GICs cause pulpal inflammatory responses. Recently, GICs containing tanninfluoride preparation (HY agent) were developed. In this study, we investigated the effect of HY agent on prostaglandin E 2 (PGE 2 ) release from GIC-stimulated rat dental pulp cells (RPC-C2A). Extracts derived from GIC disks were used with HY(+) and without HY(-) agent. After treatment with GIC extracts, ATP contents, COX-2 mRNA and protein expression in RPC-C2A cells, and PGE 2 production in culture media were analyzed. HY agent suppressed HY(-)-stimulated PGE 2 release from RPC-C2A cells, as well as COX-2 mRNA and protein expression. Moreover, tannic acid attenuated COX-2 mRNA induced by HY(-) extract in a dose-dependent manner. Taken together, these results suggest that tannic acid in HY agent may suppress GIC-induced production of PGE 2 by inhibition of COX-2 expression in dental pulp cells.

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Section: Discussionmentioning

confidence: 99%

Tannin-fluoride preparation attenuates prostaglandin E2 production by dental pulp cells

et al. 2011

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Long-term diabetes impairs repopulation of hematopoietic progenitor cells and dysregulates the cytokine expression in the bone marrow microenvironment in mice

et al. 2010

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Diabetes is characterized by a chronic stage of hyperglycemia associated with endothelial progenitor cell dysfunction and reduced neovascularization in response to tissue ischemia. The underlying mechanisms are not entirely clear. The bone marrow niches provide the essential microenvironment for maintenance of stem cell function in the bone marrow. A disturbed stem cell niche might lead to stem cell dysfunction, thereby, impairing progenitor cell-dependent vascular repair. Therefore, we investigated the effects of streptozotocin-induced diabetes on the bone marrow stem cell niches and stem cell function in mice. Here, we show that long-term diabetes induced a reduction in Lin⁻Sca-1(+)c-kit(+) hematopoietic progenitor cells and reduced the repopulation capacity in a competitive engraftment experiment. Consistently, the expression of Bmi1, which prevents hematopoietic progenitor cell senescence, was significantly reduced in diabetic bone marrow cells. To address the mechanism underlying the progenitor cell dysfunction, we analyzed the composition of the stem cell niche and the cytokine environment. Although the morphology of the vascular and endosteal niche was not affected by diabetes, diabetic mice showed a significant deterioration of cytokine expression patterns in the bone marrow. In summary, these data indicate that diabetes imposes a long-term effect on the stem cell niche and affects important hematopoietic progenitor cell functions in mice.

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Detection of pain-related molecules in the subchondral bone of osteoarthritic knees

et al. 2009

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Knee pain is predominant among osteoarthritis (OA) patients, but the mechanism is poorly understood. We investigated subchondral bone as a source of OA knee pain using immunohistochemistry. Fifteen medial-type OA knees with minimum involvement of the lateral compartment determined by X-ray as well as magnetic resonance imaging that received total knee arthroplasty (TKA) were involved. Each pair of the medial femoral condyle (MFC) and lateral femoral condyle (LFC) was compared obtained at the time of TKA. Osteocartilaginous MFC and LFC specimens were histologically examined and stained with antibodies against cyclooxygenase 1 (Cox-1), cyclooxygenase 2 (Cox-2), substance P, tumor necrosis factor-alpha (TNF-alpha), and neuron-specific class III beta-tubulin (TUJ1), a pan-neuronal marker. Formation of cystic lesions was more frequently seen in the MFC. The lesions were composed of vascular endothelial cells, osteoclasts, and mononuclear cells and were present in similar proportions between the MFC and the LFC. Four out of 15 MFC specimens were positive for Cox-1, 15 for Cox-2, and 13 for TNF-alpha. No LFC specimens were positive for any antibodies. Substance P-positive and TUJ1-positive fibers were found in the subchondral area of the MFC, but not in the LFC. Pathological changes in the subchondral bone can be a source of knee pain, which was detectable by the positive immunoreactivity of substance P, Cox-2, TNF-alpha, and TUJ1, in the subchondral bone of affected compartments. The relatively immediate reduction in pain obtained by TKA might account for the involvement of the subchondral bone in knee pain because most of the affected subchondral plate is excised in TKA (debridement effect of TKA).

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Proinflammatory Cytokine Expression in Cyclooxygenase-2–deficient Primary Osteoblasts

Cited by 5 publications

References 31 publications

Tannin-fluoride preparation attenuates prostaglandin E2 production by dental pulp cells

Tannin-fluoride preparation attenuates prostaglandin E2 production by dental pulp cells

Long-term diabetes impairs repopulation of hematopoietic progenitor cells and dysregulates the cytokine expression in the bone marrow microenvironment in mice

Detection of pain-related molecules in the subchondral bone of osteoarthritic knees

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