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1

Exogenous sphingosine 1-phosphate and sphingosylphosphorylcholine do not stimulate phospholipase D in C6 glioma cells

100%
Dygas A., Sidorko M., Bobeszko M., Baranska J.
Acta Biochimica Polonica
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1999
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tom 46
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nr 1
In the present study we investigate the effect of exogenous sphingosine, sphingosine 1-phosphate and sphingosylphosphorylcholine on phospholipase D (PLD) activity in glioma C6 cells. The cells were prelabeled with [1-14C]palmitic acid and PLD-mediated synthesis of [14C]phosphatidylethanol was measured. Sphingosine 1-phosphate and sphingosylphosphorylcholine did not stimulate [14C]phosphatidyl-ethanol formation either at low (0.1-10 μM) or high (25-100 μM) concentrations. On the other hand, sphingosine at concentrations of 100-250 μM strongly stimulated PLD activity as compared to the effect of phorbol ester, 12-O-tetradecanoylphorbol 13-acetate (TPA), known as a PLD activator. The effect of TPA on PLD is linked to the activation of protein kinase C. The present study also shows that sphingosine additively enhances TPA-mediated PLD activity. This is in contrast to the postulated role of sphingosine as a protein kinase C inhibitor. These results demonstrate that in glioma C6 cells sphingosine not only affects PLD independently of its effect on protein kinase C, but also is unable to block TPA-mediated PLD activity.
2

Ceramides and sphingosine-1-phosphate in molecular mechanisms of neuronal cell death

86%
Czubowicz K., Strosznajder R. P.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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nr 1
Ceramides, bioactive members of the sphingolipids can be generated by de novo synthesis, sphingomyelin hydrolysis and by acylation of sphingosine. Ceramides are known to regulate several cellular processes, including differentiation, growth suppression, cell senescence and apoptosis. The ceramide levels increased in several pathological conditions such as brain ischemia, hypoglycemia, inflammation and in neurodegenerative disorders. Sphingosine, a metabolite of ceramide is phosphorylated by sphingosine kinases (Sphk type 1and 2) to sphingosine-1-phosphate (S1P). Sphingosine kinases are critical regulators of the sphingolipid biostat. The aim of this study was to investigate the role of ceramide and S1P in molecular mechanisms of neuronal cells death. The human neuroblastoma cell line (SH-SY5Y) was exposed to cell-permeable C2-ceramide. Ceramide decreased the viability of SH-SY5Y cells in concentration dependent manner. The intracellular free radical generation after ceramide treatment was about 3-fold higher comparing to control. Concomitantly our study indicated that ceramide induced poly(ADP-ribose) polymerase-1 (PARP-1) activation and decreased the level of apoptosis inducing factor (AIF) in mitochondria. Ceramide diminished the expression and level of anti-apoptotic Bcl-2 protein. PARP-1 inhibitor enhanced the level of Bcl-2 protein and cells survival keeping the level of AIF in mitochondria unchanged. The recent studies indicated that ERK1/2 are involved directly in regulation of PARP-1 activity. The specific inhibitor of these kinases protected cells against death evoked by ceramide in our experimental conditions. Moreover, our study indicated, that sphingosine-1-phosphate (S1P) increased Bcl-2 gene expression and SH-SY5Y cells survival after ceramide treatment. Summarizing, our data present that PARP-1 inhibitor and sphingosine-1-phosphate (S1P) through modulation of anti-apoptotic proteins protect mitochondria and neuronal cells against death evoked by ceramide. Supported by statutory budget of MRC and NCN Grant 5870/PO1/2011/40
3

Sphingosine, sphingosylphosphorylcholine and sphingosine 1-phosphate modulate phosphatidylserine homeostasis in glioma C6 cells

86%
Wojcik M., Baranska J.
Acta Biochimica Polonica
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1999
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tom 46
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nr 1
The effect of sphingosine, sphingosylphosphorylcholine and sphingosine 1-phosphate on L-[U-14C]serine incorporation into phosphatidylserine and phosphatidylserine-derived phosphatidylethanolamine was investigated in intact glioma C6 cells. Sphingosine, sphingosylphosphorylcholine and sphingosine 1-phosphate are potent signalling molecules which, due to their physicochemical features, may function as amphiphilic compounds. It has been found that sphingosine and sphingosylphosphorylcholine (amphiphilic cations) significantly increase [14C]phosphatidylserine synthesis and decrease the amount of 14C-labeled phosphatidylethanolamine. Sphingosine 1-phosphate (an amphiphilic anion) was without effect on phosphatidylserine synthesis but, similarly as sphingosine and sphingosylphosphorylcholine, reduced the conversion of phosphatidylserine to phosphatidylethanolamine. These results strongly suggest that sphingosine, sphingosylphosphorylcholine and sphingosine 1-phosphate can modulate cellular phospholipid homeostasis by stimulation of phosphatidylserine synthesis and an interference with phosphatidylserine decarboxylase.
4
Content available remote

Ozonation of human blood increases sphingosine-1-phosphate in plasma

72%
Boczkowska-Radziwon B., Chabowska A. M., Blachnio-Zabielska A., Lukaszuk B., Lipska A., Chabowski A., Radziwon P.
Journal of Physiology and Pharmacology
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2015
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tom 66
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nr 2
5

Chronic increases in sphingosine kinase-1 activity induce a pro-inflammatory, pro-angiogenic phenotype in endothelial cells

72%
Limaye V., Xia P., Hahn C., Smith M., Vadas M. A., Pitson S. M., Gamble J. R.
Cellular and Molecular Biology Letters
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2009
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tom 14
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nr 3
424-441
Sphingosine kinase-1 (SK1) promotes the formation of sphingosine-1-phosphate (S1P), which has potent pro-inflammatory and pro-angiogenic effects. We investigated the effects of raised SK1 levels on endothelial cell function and the possibility that this signaling pathway is activated in rheumatoid arthritis. Human umbilical vein endothelial cells with 3- to 5-fold SK1 (ECSK) overexpression were generated by adenoviral and retroviralmediated gene delivery. The activation state of these cells and their ability to undergo angiogenesis was determined. S1P was measured in synovial fluid from patients with RA and OA. ECSK showed an enhanced migratory capacity and a stimulated rate of capillary tube formation. The cells showed constitutive activation as evidenced by the induction of basal VCAM-1 expression, and further showed a more augmented VCAM-1 and E selectin response to TNF compared with empty vector control cells (ECEV). These changes had functional consequences in terms of enhanced neutrophil binding in the basal and TNFstimulated states in ECSK. By contrast, over-expression of a dominant-negative SK inhibited the TNF-induced VCAM-1 and E selectin and inhibited PMN adhesion, confirming that the observed effects were specifically mediated by SK. The synovial fluid levels of S1P were significantly higher in patients with RA than in those with OA. Small chronic increases in SK1 activity in the endothelial cells enhance the ability of the cells to support inflammation and undergo angiogenesis, and sensitize the cells to inflammatory cytokines. The SK1 signaling pathway is activated in RA, suggesting that manipulation of SK1 activity in diseases of aberrant inflammation and angiogenesis may be beneficial.
6

Sphingosine-1-phosphate: a master regulator of lymphocyte egress and immunity

72%
Simmons S., Ishii M.
Archivum Immunologiae et Therapiae Experimentalis
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2014
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tom 62
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nr 2
7

The effects of markedly raised intracellular sphingosine kinase-1 activity in endothelial cells

72%
Limaye V., Vadas M. A., Pitson S. M., Gamble J. R.
Cellular and Molecular Biology Letters
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2009
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tom 14
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nr 3
411-423
The enzyme sphingosine kinase-1 (SK1) promotes the formation of sphingosine-1-phosphate (S1P), which is an important survival factor for endothelial cells (EC). Modest increases in intracellular SK1 activity in the EC are known to confer a survival advantage upon the cells. Here, we investigated the effects of more dramatic increases in intracellular SK1 in the EC. We found that these cells show reduced cell survival under conditions of stress, enhanced caspase-3 activity, cell cycle inhibition, and cell-cell junction disruption. We propose that alterations in the phosphorylation state of the enzyme may explain the differential effects on the phenotype with modest versus high levels of enforced expression of SK1. Our results suggest that SK1 activity is subject to control in the EC, and that this control may be lost in conditions involving vascular regression.
8

The role of the lysophospholipid sphingosine 1-phosphate in immune cell biology

72%
Von Wenckstern H., Zimmermann K., Kleuser B.
Archivum Immunologiae et Therapiae Experimentalis
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2006
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tom 54
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nr 4
9
Content available remote

Cardioprotective role of sphingosine-1-phosphate

58%
Knapp M.
Journal of Physiology and Pharmacology
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2011
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tom 62
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nr 6
10

Immune regulation by sphingosine 1-phosphate and its receptors

58%
Bode C., Graler M. H.
Archivum Immunologiae et Therapiae Experimentalis
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2012
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tom 60
|
nr 1
11

The role of sphingosine kinases/sphingosine-1-phosphate in the regulation of alpha-synuclein and amyloid beta precursor protein secretion. Implications for neurodegenerative disorders

58%
Jesko H., Okada T., Nakamura S., Strosznajder R. P.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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nr 1
Sphingolipid deregulation may be an important factor of age-related neuronal stress vulnerability. Current data suggests potential links between sphingosine kinases (SphK1&2), their product sphingosine1-phosphate (S1P) and age-related protein conformation diseases. The aim of this study was to investigate a possible role of SphKs in alpha-synuclein (ASN) and amyloid beta (ABeta) precursor protein (APP) level and secretion. The studies were carried out using human SH-SY5Y neuroblastoma cell line stably transfected with the human gene for α-synuclein (ASNwt). Sphingosine kinase inhibitor (SKI) significantly increased ASN secretion in concentration-dependent manner. S1P also displayed similar influence. Neither compound exerted any significant effect on the ASN protein level. S1P may act via cell surface receptors or as an intracellular second messenger. The similar effect of S1P and SphK inhibitors on ASN secretion may suggest that the regulation of its release is critically dependent on the varied (intra)cellular targets of SphKs and downstream signaling pathways. We have found that stable human ASNwt expression in SH-SY5Y cells caused a three-fold, significant increase of the cellular APP level. In ASN-transfected cells S1P enhanced APP secretion and reduced its intracellular level. This could be linked to the recently reported effect of S1P on secretase beta activity. Inhibition of SphKs significantly decreased APP secretion. In summary our data indicates that endogenous ASN regulates APP level in SH-SY5Y cells and that sphingolipids play a crucial role in the secretion of ASN and APP. These processes may have significant impact on neuronal survival and health.
12

Siponimod (Mayzent) downregulates RhoA and cell surface expression of the S1P1 and CX3CR1 receptors in mouse RAW 264.7 macrophages

58%
Uosef A., Vaughn N., Chu X., Elshawwaf M., Abelelshafy A. A. A., Elsaid K. M. K., Ghobrial R. M., Kloc M.
Archivum Immunologiae et Therapiae Experimentalis
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2020
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tom 68
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nr 3
13

Sphingosine 1-phosphate is a blood constituent released from activated platelets, possibly playing a variety of physiological and pathophysiological roles

58%
Igarashi Y., Yatomi Y.
Acta Biochimica Polonica
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1998
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tom 45
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nr 2
We have found that sphingosine 1-phosphate (Sph-1-P) acts as an autocrine stimulator of platelets, being abundantly stored in platelets and released extracellularly, and that its exogenous addition induces platelet activation (Yatomi et al., Blood 1995, 86, 193-202) through a specific receptor on the platelet surface (Yatomi et al., J. Biol. Chem. 1997, 272, 5291-5297). Very recently, we identified Sph-1-P as a normal constituent of human plasma and serum. Sph-1-P levels in plasma and serum were 191±79 and 484±82 pmol/ml (mean ±S.D., n = 8), respectively. Platelets are most likely the source of Sph-1-P discharged during blood clotting, since they abundantly store Sph-1-P as compared with other blood cells, and release considerable amounts of stored Sph-1-P extracellularly upon stimulation. The Sph-1-P released from activated platelets may be involved in a variety of physiological processes, including thrombosis, atherosclerosis, and wound healing. Moreover, we often observed that Sph-1-P injection into mice (iv., 10 mg/kg) caused immediate rigor and death. This may be related to the recent observations from an other laboratory that nanomolar concentrations of Sph-1-P affected atrial myocyte K+ channel. These observations taken together strongly suggest pathophysiological roles of the released Sph-1-P in the blood. As one example, we found that Sph-1-P content in the plasma of platelet concentrates correlated with poor platelet increments after transfusion and with the occurence of transfusion reactions in patients.
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