Immunohistochemical localization of the prostacyclin receptor (IP) human bone

Fortier, Isabelle; Patry, Christian; Lora, Maximilien; Samadfan, R.; Brum‐Fernandes, Artur J. de

doi:10.1054/plef.2001.0292

Cited by 17 publications

(17 citation statements)

References 28 publications

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“…PGI 2 interacts with a specific receptor, IP, which is a G protein-coupled cell surface receptor. The IP receptor was detected in fetal bone and osteoblasts (Fortier et al, 2001). Although the IP receptor was expressed in both OPLL cells and non-OPLL cells, beraprost only increased the ALP mRNA expression in OPLL cells.…”

Section: Discussionmentioning

confidence: 92%

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Role of Prostaglandin I₂in the Gene Expression Induced by Mechanical Stress in Spinal Ligament Cells Derived from Patients with Ossification of the Posterior Longitudinal Ligament

Ohishi

Furukawa²,

Iwasaki³

et al. 2003

J Pharmacol Exp Ther

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Ossification of the posterior longitudinal ligament of the spine (OPLL) is characterized by ectopic bone formation in the spinal ligaments, and mechanical stress has been suggested to play an important role in the progression of OPLL. To identify the genes that participate in OPLL, the differential display reverse transcription-polymerase chain reaction (RT-PCR) method was used. A 283-base pair cDNA fragment corresponding to prostaglandin I 2 (PGI 2 ) synthase was highly expressed in OPLL cells compared with non-OPLL cells. To examine the effect of mechanical stress on the expression of PGI 2 synthase, cells were subjected to uniaxial cyclic stretch (0.5 Hz, 20% stretch), and PGI 2 synthase mRNA expression was assessed by quantitative RT-PCR. Cyclic stretch induced an increase in PGI 2 synthase in OPLL cells in a time-dependent manner, whereas no change was observed in non-OPLL cells. Cyclic stretch for 9 h also induced a 2.86ϫ increase in PGI 2 production. Beraprost (a stable PGI 2 analog) and dibutyryl cAMP (a membrane-permeable cAMP analog) increased the mRNA expression of alkaline phosphatase (ALP) as a marker for osteogenic differentiation up to 240 and 200%, respectively, in OPLL cells, whereas no change was observed in non-OPLL cells. The increases in ALP mRNA induced by beraprost and cyclic stretch were both inhibited by SQ22536, a potent adenylate cyclase inhibitor. These data suggest that the increase in PGI 2 synthase induced by mechanical stress plays a key role in the progression of OPLL, at least in part through the induction of osteogenic differentiation in spinal ligament cells via the PGI 2 /cAMP system.

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Section: Discussionmentioning

confidence: 92%

“…Among the natural prostaglandins, PGI 2 is the major component produced in bone metabolism and the most potent inhibitor of bone resorption (Fortier et al, 2001). PGI 2 is converted from prostaglandin H 2 by PGI 2 synthase, the key enzyme in PGI 2 production.…”

Section: Discussionmentioning

confidence: 99%

Role of Prostaglandin I₂in the Gene Expression Induced by Mechanical Stress in Spinal Ligament Cells Derived from Patients with Ossification of the Posterior Longitudinal Ligament

Ohishi

Furukawa²,

Iwasaki³

et al. 2003

J Pharmacol Exp Ther

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“…Similarly, osteocytic cells in vitro were shown to increase COX-2 expression and prostaglandin production in response to diverse mechanical stimuli including fluid flow [103, 104], substrate deformation [105] and hydrostatic pressure [34]. Of the prostaglandins, PGE 2 is the most extensively studied with respect to bone anabolic effects, although prostacyclin (PGI 2 ) has also been reported to have similar actions [106, 107]. Sorting out pathways of prostaglandin signaling between osteocytic and osteoblastic cell populations presents problems, particularly in situ , since both osteoblasts and osteocytes produce prostaglandins.…”

Section: Osteocyte-osteoblast Communicationmentioning

confidence: 99%

Osteocytes: Master Orchestrators of Bone

et al. 2013

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Osteocytes comprise the overwhelming majority of cells in bone and are its only true “permanent” resident cell population. In recent years, conceptual and technological advances on many fronts have helped to clarify the role osteocytes play in skeletal metabolism and the mechanisms they use to perform them. The osteocyte is now recognized as a major orchestrator of skeletal activity, capable of sensing and integrating mechanical and chemical signals from their environment to regulate both bone formation and resorption. Recent studies have established that the mechanisms osteocytes use to sense stimuli and regulate effector cells (e.g. osteoblasts and osteoclasts) are directly coupled to the environment they inhabit – entombed within the mineralized matrix of bone and connected to each other in multicellular networks. Communication within these networks is both direct (via cell-cell contacts at gap junctions) and indirect (via paracrine signaling by secreted signals). Moreover, the movement of paracrine signals is dependent on movement of both solutes and fluid through the space immediately surrounding the osteocytes (i.e. the Lacunar-Canalicular System, LCS). Finally, recent studies have also shown that the regulatory capabilities of osteocytes extend beyond bone to include a role in endocrine control of systemic phosphate metabolism. This review will discuss how a highly productive combination of experimental and theoretical approaches has managed to unearth these unique features of osteocytes and bring to light novel insights into the regulatory mechanisms operating in bone.

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“…A potential well-recognized risk factor facilitating hypocalcemia is chronic kidney disease with a clearance <50 mL/min (as well as end stage renal disease) [4-9]. In addition, it has been shown that prostacyclin itself has an effect on bone modelling: it inhibits osteoclasts, and an overproduction of prostacyclin can reduce osteoblast differentiation [10, 11]. Since both denosumab and prostacyclin (which both inhibit osteoclast activity) were used in this patient, we assume that the risk of inducing hypocalcemia may have been even higher.…”

Section: Discussionmentioning

confidence: 99%

Hypocalcemia after Denosumab in a Pulmonary Hypertension Patient Receiving Epoprostenol

et al. 2017

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We report the case of a 50-year-old woman with anorexigen-induced pulmonary arterial hypertension treated with epoprostenol, who presented with Trousseau’s sign, leading to the diagnosis of severe hypocalcemia for which substitution was started (initially orally, followed by intravenous substitution). After further analysis, we assume that epoprostenol-induced diarrhea caused malabsorption (as other reasons were excluded), leading to nutritional osteomalacia with secondary hyperparathyroidism. We discovered that even more severe hypocalcemia was induced by the treatment with the anti-osteoporotic drug denosumab, which was started after the diagnosis of osteoporosis on bone densitometry. In our opinion, clinicians have to be aware that in patients with malabsorption, antiresorptive therapy can induce dangerous and even life-threatening hypocalcemia, even in patients with normal renal function.

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Immunohistochemical localization of the prostacyclin receptor (IP) human bone

Cited by 17 publications

References 28 publications

Role of Prostaglandin I₂in the Gene Expression Induced by Mechanical Stress in Spinal Ligament Cells Derived from Patients with Ossification of the Posterior Longitudinal Ligament

Role of Prostaglandin I₂in the Gene Expression Induced by Mechanical Stress in Spinal Ligament Cells Derived from Patients with Ossification of the Posterior Longitudinal Ligament

Osteocytes: Master Orchestrators of Bone

Hypocalcemia after Denosumab in a Pulmonary Hypertension Patient Receiving Epoprostenol

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Immunohistochemical localization of the prostacyclin receptor (IP) human bone

Cited by 17 publications

References 28 publications

Role of Prostaglandin I2in the Gene Expression Induced by Mechanical Stress in Spinal Ligament Cells Derived from Patients with Ossification of the Posterior Longitudinal Ligament

Role of Prostaglandin I2in the Gene Expression Induced by Mechanical Stress in Spinal Ligament Cells Derived from Patients with Ossification of the Posterior Longitudinal Ligament

Osteocytes: Master Orchestrators of Bone

Hypocalcemia after Denosumab in a Pulmonary Hypertension Patient Receiving Epoprostenol

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Role of Prostaglandin I₂in the Gene Expression Induced by Mechanical Stress in Spinal Ligament Cells Derived from Patients with Ossification of the Posterior Longitudinal Ligament

Role of Prostaglandin I₂in the Gene Expression Induced by Mechanical Stress in Spinal Ligament Cells Derived from Patients with Ossification of the Posterior Longitudinal Ligament