Augmented prostaglandin E 2 generation resulting from increased activities of cytosolic and secretory phospholipase A 2 and induction of cyclooxygenase-2 in interleukin-1 β -stimulated rat calvarial cells during the mineralizing phase

Higashi, Sayumi; Ohishi, Hirotaka; Kudo, Ichiro

doi:10.1007/s000110050566

Cited by 21 publications

(12 citation statements)

References 24 publications

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“…These data are in agreement with IL-1␤-induced activation of MAPKs (Hungness et al, 2002;Parker et al, 2002) and cPLA 2 (Beasley, 1999;Higashi et al, 2000) in variety of cells. Our data suggest that H 2 O 2 production induced by shortperiod incubation with IL-1␤ does not depend on activation of NF-B, even though NF-B may be activated by IL-1␤ (Janssen- Heininger et al, 2000;Ganster et al, 2001).…”

Section: Discussionsupporting

confidence: 89%

Interleukin 1β-Induced Production of H₂O₂Contributes to Reduced Sigmoid Colonic Circular Smooth Muscle Contractility in Ulcerative Colitis

Cao¹,

Vrees²,

Potenti³

et al. 2004

J Pharmacol Exp Ther

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We have shown that neurokinin A-induced contraction of human sigmoid circular muscle (HSCM) is reduced in patients with ulcerative colitis and that interleukin (IL)-1␤ may play a role in this change. We now examine changes in the signal transduction pathway mediating neurokinin A-induced contraction of HSCM and explore the role of IL-1␤ and of H 2 O 2 in these changes. In Fura 2-AM-loaded ulcerative colitis HSCM cells, neurokinin A-and caffeine-induced peak Ca 2ϩ increase and cell shortening were significantly reduced. In normal cells, neurokinin A-induced contraction was decreased by protein kinase

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Section: Discussionsupporting

confidence: 89%

Interleukin 1β-Induced Production of H₂O₂Contributes to Reduced Sigmoid Colonic Circular Smooth Muscle Contractility in Ulcerative Colitis

Cao¹,

Vrees²,

Potenti³

et al. 2004

J Pharmacol Exp Ther

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“…Additional studies in the authors' lab have pursued this line of reasoning and further described the role of phospholipase A 2 in the response of osteoblasts to Ti surface roughness and 1,25(OH) 2 D 3 , 44,45 while others have reported on the involvement of phospholipase A 2 and COX-2 in augmenting PGE 2 production during mineralization of rat calvarial cells. 46 Studies have shown that MG63 cells cultured on titanium disks of increasing roughness, similar to those used in the current study, produce increased amounts of PGE 2 . 18 On smooth Ti, the cultures were found to produce 50 pg/mL (¼ 0.7 nM) of PGE 2 , while those on rough Ti produced 160 pg/mL (¼ 4.5 nM).…”

Section: Discussionmentioning

confidence: 81%

Arachidonic Acid and Prostaglandin E2 Influence Human Osteoblast (MG63) Response to Titanium Surface Roughness

Dean¹,

Campbell

Gruwell

et al. 2008

Journal of Oral Implantology

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Prior studies have shown that implant surface roughness affects osteoblast proliferation, differentiation, matrix synthesis, and local factor production. Further, cell response is modulated by systemic factors, such as 1,25(OH)2D3 and estrogen as well as mechanical forces. Based on the fact that peri-implant bone healing occurs in a site containing elevated amounts of prostaglandin E2 (PGE2), the hypothesis of the current study is that PGE2 and arachidonic acid (AA), the substrate used by cyclooxygenase to form PGE2, influence osteoblast response to implant surface roughness. To test this hypothesis, 4 different types of commercially pure titanium (cpTi) disks with surfaces of varying roughness (smooth Ti, R(a) 0.30 microm; smooth and acid etched Ti [SAE Ti], R(a) 0.40 microm; rough Ti, R(a) 4.3 microm; rough and acid etched Ti [RAE Ti], R(a) 4.15 (microm) were prepared. MG63 osteoblasts were seeded onto the surfaces, cultured to confluence, and then treated for the last 24 hours of culture with AA (0, 0.1, 1, and 10 nM), PGE2 (0, 1, 10, 25, and 100 nM), or the general cyclooxygenase inhibitor indomethacin (0 or 100 nM). At harvest, the effect of treatment on cell proliferation was assessed by measuring cell number and [3H]-thymidine incorporation, and the effect on cell differentiation was determined by measuring alkaline phosphatase (ALP) specific activity. The effect of AA and PGE2 on cell number was somewhat variable but showed a general decrease on plastic and smooth surfaces and an increase on rough surfaces. In contrast, [3H]-thymidine incorporation was uniformly decreased with treatment on all surfaces. ALP demonstrated the most prominent effect of treatment. On smooth surfaces, AA and PGE2 dose-dependently increased ALP, while on rough surfaces, treatment dose-dependently decreased enzyme specific activity. Indomethacin treatment had either no effect or a slightly inhibitory effect on [3H]-thymidine incorporation on all surfaces. In contrast, indomethacin inhibited ALP on smooth surfaces and stimulated ALP on rough. Taken together, the results indicate that both AA and PGE2 influence osteoblast response by promoting osteoblast differentiation on smooth surfaces, while inhibiting it on rough surfaces. Because implants with rough surfaces are acknowledged to be superior to those with smooth surfaces, these results suggest that use of nonsterioidal anti-inflammatory drugs to block PGE2 production and reduce inflammation may be beneficial in the postoperative period after implant placement. They also indicate that manipulation of the AA metabolic pathway may offer a new therapeutic approach for modulating bone healing after implant placement. Because peri-implant healing takes place in a complex cellular environment quite different from the one used in the present study, additional work will be necessary to substantiate these possibilities.

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“…VOL. 21,2001 PLIP INTERACTS WITH cPLA 2 AND POTENTIATES APOPTOSIScPLA 2 expression has also been closely linked to PGE 2 generation (2,11,32,49,53), which has been shown to have both pro- (17,49,60) and anti-(58) apoptotic effects. We compared PGE 2 generation in Ad-PLIP-infected cPLA 2 ϩ/ϩ and cPLA 2 Ϫ/Ϫ mesangial cells incubated in serum-free medium for 48 h. PLIP expression markedly increases PGE 2 production in cPLA 2 ϩ/ϩ but not cPLA 2 Ϫ/Ϫ cells (Fig.…”

Section: Resultsmentioning

confidence: 99%

PLIP, a Novel Splice Variant of Tip60, Interacts with Group IV Cytosolic Phospholipase A₂, Induces Apoptosis, and Potentiates Prostaglandin Production

Force

Yoon

et al. 2001

Molecular and Cellular Biology

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Augmented prostaglandin E 2 generation resulting from increased activities of cytosolic and secretory phospholipase A 2 and induction of cyclooxygenase-2 in interleukin-1 β -stimulated rat calvarial cells during the mineralizing phase

Abstract: Augmented PGE2 production by mineralizing osteoblasts after IL-1beta treatment, and the involvement of IL-1beta-induced cPLA2, sPLA2, COX-2 and PGE synthase activities in this phenomenon were demonstrated.

Cited by 21 publications

References 24 publications

Interleukin 1β-Induced Production of H₂O₂Contributes to Reduced Sigmoid Colonic Circular Smooth Muscle Contractility in Ulcerative Colitis

Interleukin 1β-Induced Production of H₂O₂Contributes to Reduced Sigmoid Colonic Circular Smooth Muscle Contractility in Ulcerative Colitis

Arachidonic Acid and Prostaglandin E2 Influence Human Osteoblast (MG63) Response to Titanium Surface Roughness

PLIP, a Novel Splice Variant of Tip60, Interacts with Group IV Cytosolic Phospholipase A₂, Induces Apoptosis, and Potentiates Prostaglandin Production

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Augmented prostaglandin E 2 generation resulting from increased activities of cytosolic and secretory phospholipase A 2 and induction of cyclooxygenase-2 in interleukin-1 β -stimulated rat calvarial cells during the mineralizing phase

Abstract: Augmented PGE2 production by mineralizing osteoblasts after IL-1beta treatment, and the involvement of IL-1beta-induced cPLA2, sPLA2, COX-2 and PGE synthase activities in this phenomenon were demonstrated.

Cited by 21 publications

References 24 publications

Interleukin 1β-Induced Production of H2O2Contributes to Reduced Sigmoid Colonic Circular Smooth Muscle Contractility in Ulcerative Colitis

Interleukin 1β-Induced Production of H2O2Contributes to Reduced Sigmoid Colonic Circular Smooth Muscle Contractility in Ulcerative Colitis

Arachidonic Acid and Prostaglandin E2 Influence Human Osteoblast (MG63) Response to Titanium Surface Roughness

PLIP, a Novel Splice Variant of Tip60, Interacts with Group IV Cytosolic Phospholipase A2, Induces Apoptosis, and Potentiates Prostaglandin Production

Contact Info

Product

Resources

About

Interleukin 1β-Induced Production of H₂O₂Contributes to Reduced Sigmoid Colonic Circular Smooth Muscle Contractility in Ulcerative Colitis

Interleukin 1β-Induced Production of H₂O₂Contributes to Reduced Sigmoid Colonic Circular Smooth Muscle Contractility in Ulcerative Colitis

PLIP, a Novel Splice Variant of Tip60, Interacts with Group IV Cytosolic Phospholipase A₂, Induces Apoptosis, and Potentiates Prostaglandin Production