Sphingosine 1-phosphate amplifies phosphoinositide hydrolysis stimulated by prostaglandin F2α in osteoblasts: involvement of p38 MAP kinase

Kozawa, Osamu; Kawamura, Hidenori

doi:10.1054/plef.2000.0166

Cited by 4 publications

(4 citation statements)

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“…(4 -8) Occupancy of plasma membrane receptors for prostaglandin F 2␣ , epidermal growth factor, platelet-derived growth factor, tumor necrosis factor, and nerve growth factor is coupled in a variety of cell types to the activation of sphingomyelinase and generation in the cytoplasm of the sphingomyelin hydrolysis product ceramide. (9 -11) Other sphingolipid actions in osteoblasts have been linked to cell proliferation, (11,12) synthesis of interleukin-6, (13) activation of members of the mitogen-activated protein (MAP) kinase family, (12,14) and stimulation of the AP-1 transcription factor. SPH and SPP are agonists of acute elevations in [Ca 2ϩ ] i in osteoblastic cells.…”

Section: Introductionmentioning

confidence: 99%

“…SPH and SPP are agonists of acute elevations in [Ca 2ϩ ] i in osteoblastic cells. (9 -11) Other sphingolipid actions in osteoblasts have been linked to cell proliferation, (11,12) synthesis of interleukin-6, (13) activation of members of the mitogen-activated protein (MAP) kinase family, (12,14) and stimulation of the AP-1 transcription factor. (15) The sphingosine (SPH) derivative sphingosylphosphorylcholine (SPC) has biological effects that mimic those of SPP, including the ability to induce Ca 2ϩ release from the ER in MC3T3-E1 cells.…”

Section: Introductionmentioning

confidence: 99%

“…However, exposure of MC3T3-E1 cells to SPH eliminated LPA-induced elevations in [Ca 2ϩ ] i despite the fact that intracellular stores had refilled after SPH addition. The Ca 2ϩ transients observed in SPH-treated cells may reflect SPH entry followed by cytoplasmic conversion to SPP, which itself can act as an intracellular lanes 1-3), Edg-3 (lanes 4 -6), Edg-5 (lanes 7-9), Edg-6 (lanes 10 -12), and Edg-8 (lanes [13][14][15] receptors. Samples of the PCR reactions were separated on a 1% agarose gel containing ethidium bromide.…”

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confidence: 99%

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A Role for G Protein-Coupled Lysophospholipid Receptors in Sphingolipid-Induced Ca2+ Signaling in MC3T3-E1 Osteoblastic Cells

Lyons

Karin

2001

Journal of Bone and Mineral Research

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Sphingolipids have been proposed to modulate cell function by acting as intracellular second messengers and through binding to plasma membrane receptors. Exposure of MC3T3-E1 osteoblastic cells to sphingosine (SPH), sphingosine-1-phosphate (SPP), or sphingosylphosphorylcholine (SPC) led to the release of Ca2+ from the endoplasmic reticulum (ER) and acute elevations in cytosolic-free Ca2+ ([Ca2+]i). Desensitization studies suggest that SPP and SPC bind plasma membrane endothelial differentiation gene (Edg) receptors for lysophosphatidic acid (LPA). Consistent with the coupling of Edg receptors to G proteins, SPP- and SPC-induced Ca2+ signaling was inhibited by pretreatment of the cells with pertussis toxin (PTx). Of the Edg receptors known to bind SPH derivatives in other cell types, MC3T3-E1 cells were found to express transcripts encoding Edg-1 and Edg-5 but not Edg-3, Edg-6, or Edg-8. In contrast to SPP and SPC, the ability of SPH to elicit [Ca2+]i elevations was affected neither by prior exposure of cells to LPA nor by PTx treatment. However, LPA-induced Ca2+ signaling was blocked in MC3T3-E1 cells previously exposed to SPH. Elevations in [Ca2+]i were not evoked by SPP or SPC in cells treated with 2-aminoethoxydiphenylborate (2-APB), an inhibitor of inositol 1,4,5-trisphosphate (IP3)-gated Ca2+ channels in the ER. No effect of 2-APB was observed on SPH-or LPA-induced [Ca2+]i elevations. The data support a model in which SPP and SPC bind Edg-1 and/or Edg-5 receptors in osteoblasts leading to the release of Ca2+ from the ER through IP3-gated channels.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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confidence: 99%

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A Role for G Protein-Coupled Lysophospholipid Receptors in Sphingolipid-Induced Ca2+ Signaling in MC3T3-E1 Osteoblastic Cells

Lyons

Karin

2001

Journal of Bone and Mineral Research

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“…Because of calcium's central role in cell signalling, it is therefore not surprising that S1P is implicated in many osteoblast functions. Indeed, S1P stimulates IL-6 synthesis in these cells in a p42/p44 MAPK dependent manner (85), induces the synthesis of heat-shock protein 27 (HSP27) via p38 activation (86), and enhances PGF2α-induced phosphoinositide hydrolysis by phospholipase C through p38 MAPK (87,88).…”

Section: Other Effect Of S1p Signalling In Osteoblastsmentioning

confidence: 99%

Sphingosine 1-phosphate (S1P) signalling: Role in bone biology and potential therapeutic target for bone repair

Sartawi

Schipani

Ryan

et al. 2017

Pharmacological Research

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The lipid mediator sphingosine 1-phosphate (S1P) affects cellular functions in most systems. Interest in its therapeutic potential has increased following the discovery of its G protein-coupled receptors and the recent availability of agents that can be safely administered in humans. Although the role of S1P in bone biology has been the focus of much less research than its role in the nervous, cardiovascular and immune systems, it is becoming clear that this lipid influences many of the functions, pathways and cell types that play a key role in bone maintenance and repair. Indeed, S1P is implicated in many osteogenesis-related processes including stem cell recruitment and subsequent differentiation, differentiation and survival of osteoblasts, and coupling of the latter cell type with osteoclasts. In addition, S1P's role in promoting angiogenesis is well-established. The pleiotropic effects of S1P on bone and blood vessels have significant potential therapeutic implications, as current therapeutic approaches for critical bone defects show significant limitations. Because of the complex effects of S1P on bone, the pharmacology of S1P-like agents and their physico-chemical properties, it is likely that therapeutic delivery of S1P agents will offer significant advantages compared to larger molecular weight factors. Hence, it is important to explore novel methods of utilizing S1P agents therapeutically, and improve our understanding of how S1P and its receptors modulate bone physiology and repair.

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Cellular Signaling by Sphingosine and Sphingosine 1-Phosphate

Pyne

Subcellular Biochemistry

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Sphingosine 1-phosphate amplifies phosphoinositide hydrolysis stimulated by prostaglandin F2α in osteoblasts: involvement of p38 MAP kinase

Cited by 4 publications

References 20 publications

A Role for G Protein-Coupled Lysophospholipid Receptors in Sphingolipid-Induced Ca2+ Signaling in MC3T3-E1 Osteoblastic Cells

A Role for G Protein-Coupled Lysophospholipid Receptors in Sphingolipid-Induced Ca2+ Signaling in MC3T3-E1 Osteoblastic Cells

Sphingosine 1-phosphate (S1P) signalling: Role in bone biology and potential therapeutic target for bone repair

Cellular Signaling by Sphingosine and Sphingosine 1-Phosphate

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