Characterization of the prostaglandin receptors in human osteoblasts in culture

Sarrazin, Patrice; Bkaily, Ghassan; Haché, Robert J.G.; Patry, Christian; Dumais, R.; Rocha, Francisco Airton Castro; Brum‐Fernandes, Artur J. de

doi:10.1054/plef.1999.0127

Cited by 28 publications

(22 citation statements)

References 29 publications

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“…PGE 2 has been demonstrated to exert both anabolic and catabolic effects depending on the activation of its specific receptor subtypes. In osteoblasts, three such receptors, EP1, EP2 and EP4, are present [33,34]. PGE 2 signalling through the EP1 receptor enhances proanabolic effects such as bone formation, whereas signalling through the EP2 and EP4 receptors induces catabolic effects on bone [35][36][37].…”

Section: Discussionmentioning

confidence: 99%

Differential modulation of RANKL isoforms by human osteoarthritic subchondral bone osteoblasts: Influence of osteotropic factors

Tat

Pelletier

Lajeunesse

et al. 2008

Bone

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Background-Osteoarthritis (OA) is the most common human joint disease. Recent studies suggest that an abnormal subchondral bone metabolism is intimately involved in the genesis of this disease. Bone remodelling is tightly regulated by a molecular triad composed of OPG/RANK/ RANKL. RANKL exists as 3 isoforms: RANKL1, 2, and 3. RANKL1 and 2 enhance osteoclastogenesis whereas RANKL3 inhibits this phenomenon. We previously reported that human OA subchondral bone osteoblasts can be discriminated into two subgroups according to their level of PGE 2 [low (L) or high (H)]. Moreover, we also showed that L-OA osteoblasts express higher levels of total RANKL compared to H-OA osteoblasts. In this study, we investigated the level of membranous RANKL, comparing L-and H-OA subchondral bone osteoblasts, as well as its modulation by osteotropic factors. The impact of the modulation of RANKL1 and 3 on the membranous RANKL level was also studied.

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Section: Discussionmentioning

confidence: 99%

Differential modulation of RANKL isoforms by human osteoarthritic subchondral bone osteoblasts: Influence of osteotropic factors

Tat

Pelletier

Lajeunesse

et al. 2008

Bone

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“…EP3. EP4 receptors are also strongly expressed in primary cultures of human osteoblasts (Sarrazin et al, 2001). In human osteoblasts, only EP4 and EP3 were observed immunohistochemically .…”

Section: Other Immune Cellsmentioning

confidence: 97%

“…Expression. EP4 receptors have been found in rats (Sarrazin et al, 2001) and mice Suzawa et al, 2000) through primary culture of osteoblasts and various osteoblastic cell lines, including MCT3T3-E1, and bone marrow stromal cell EP4 Signaling cultures (Suda et al, 1996;Weinreb et al, 1999Weinreb et al, , 2001Sarrazin et al, 2001;). Miyaura et al (2000) demonstrated that mouse osteoblasts isolated from calvariae expressed transcripts of all four receptors, ranked according to expression level as follows: EP4 .…”

Section: Other Immune Cellsmentioning

confidence: 99%

The Prostanoid EP4 Receptor and Its Signaling Pathway

Yokoyama

Iwatsubo²,

Umemura³

et al. 2013

Pharmacol Rev

223

257

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“…DP1 receptor (387 bp) was amplified by the primer set 5V -GCAACCTCTATGCGATGCAC-3Vand 5V -GAATTGCTGCACCGGCTCCT-3Vas described by Sarrazin et al (22). DP2 receptor (309 bp), otherwise known as CRTH2 receptor, was amplified by the primer set 5V -CCTCTGT-GCC CAGAGCC CC ACGATGTCGGC-3V and 5V -CACGGCC AAGA-AGTAGGTGAAGAAG-3V as described by Nagata et al (23).…”

Section: Introductionmentioning

confidence: 99%

Suppression of Prostate Tumor Cell Growth by Stromal Cell Prostaglandin D Synthase–Derived Products

Kim

Yang²,

Suraokar

et al. 2005

Cancer Research

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Stromal-epithelial interactions and the bioactive molecules produced by these interactions maintain tissue homeostasis and influence carcinogenesis. Bioactive prostaglandins produced by prostaglandin synthases and secreted by the prostate into seminal plasma are thought to support reproduction, but their endogenous effects on cancer formation remain unresolved. No studies to date have examined prostaglandin enzyme production or prostaglandin metabolism in normal prostate stromal cells. Our results show that lipocalin-type prostaglandin D synthase (L-PGDS) and prostaglandin D 2 (PGD 2 ) metabolites produced by normal prostate stromal cells inhibited tumor cell growth through a peroxisome proliferator-activated receptor ; (PPAR;)-dependent mechanism. Enzymatic products of stromal cell L-PGDS included high levels of PGD 2 and 15-deoxy-# 12,14 -PGD 2 but low levels of 15-deoxy-# 12,14 -prostaglandin J 2 . These PGD 2 metabolites activated the PPAR; ligand-binding domain and the peroxisome proliferator response element reporter systems. Thus, growth suppression of PPAR;-expressing tumor cells by PGD 2 metabolites in the prostate microenvironment is likely to be an endogenous mechanism involved in tumor suppression that potentially contributes to the indolence and long latency period of this disease. (Cancer Res 2005; 65(14): 6189-98)

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Characterization of the prostaglandin receptors in human osteoblasts in culture

Cited by 28 publications

References 29 publications

Differential modulation of RANKL isoforms by human osteoarthritic subchondral bone osteoblasts: Influence of osteotropic factors

Differential modulation of RANKL isoforms by human osteoarthritic subchondral bone osteoblasts: Influence of osteotropic factors

The Prostanoid EP4 Receptor and Its Signaling Pathway

Suppression of Prostate Tumor Cell Growth by Stromal Cell Prostaglandin D Synthase–Derived Products

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