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Journal articles on the topic 'S1P receptor antagonists'

Author: Grafiati

Published: 14 March 2023

Last updated: 31 July 2025

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1

Sumida, Grant M., and W. Daniel Stamer. "S1P2 receptor regulation of sphingosine-1-phosphate effects on conventional outflow physiology." American Journal of Physiology-Cell Physiology 300, no. 5 (2011): C1164—C1171. http://dx.doi.org/10.1152/ajpcell.00437.2010.

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Elevated intraocular pressure is the main risk factor in primary open-angle glaucoma, involving an increased resistance to aqueous humor outflow in the juxtacanalicular region of the conventional outflow pathway which includes the trabecular meshwork (TM) and the inner wall of Schlemm's canal (SC). Previously, sphingosine-1-phosphate (S1P) was shown to decrease outflow facility in porcine and human eyes, thus increasing outflow resistance and intraocular pressure. Owing to S1P's known effect of increasing barrier function in endothelial cells and the robust expression of the S1P1 receptor on t

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Zhang, Dong Dong, Bona Linke, Jing Suo, et al. "Antinociceptive effects of FTY720 during trauma-induced neuropathic pain are mediated by spinal S1P receptors." Biological Chemistry 396, no. 6-7 (2015): 783–94. http://dx.doi.org/10.1515/hsz-2014-0276.

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Abstract FTY720 (fingolimod) is, after its phosphorylation by sphingosine kinase (SPHK) 2, a potent, non-selective sphingosine-1-phosphate (S1P) receptor agonist. FTY720 has been shown to reduce the nociceptive behavior in the paclitaxel model for chemotherapy-induced neuropathic pain through downregulation of S1P receptor 1 (S1P1) in microglia of the spinal cord. Here, we investigated the mechanisms underlying the antinociceptive effects of FTY720 in a model for trauma-induced neuropathic pain. We found that intrathecal administration of phosphorylated FTY720 (FTY720-P) decreased trauma-induc

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Lukas, Susan, Lori Patnaude, Sokol Haxhinasto, et al. "No Differences Observed among Multiple Clinical S1P1 Receptor Agonists (Functional Antagonists) in S1P1 Receptor Down-regulation and Degradation." Journal of Biomolecular Screening 19, no. 3 (2013): 407–16. http://dx.doi.org/10.1177/1087057113502234.

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Sphingosine-1-phosphate (S1P) is a bioactive metabolite with pleiotropic effects on multiple cellular processes in health and disease. Responses elicited by S1P are a result of binding to five specific G-protein–coupled receptors. We have developed multiple assays to systematically study the downstream signaling of these receptors, including early events such as direct receptor activation (GTPγS) as well as more distal events such as S1P1 receptor degradation. Employing such assays, we have characterized and compared multiple S1P1 agonists that are in clinical development including FTY720, BAF

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Hafizi, Redona, Faik Imeri, Roland H. Wenger та Andrea Huwiler. "S1P Stimulates Erythropoietin Production in Mouse Renal Interstitial Fibroblasts by S1P1 and S1P3 Receptor Activation and HIF-2α Stabilization". International Journal of Molecular Sciences 22, № 17 (2021): 9467. http://dx.doi.org/10.3390/ijms22179467.

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Erythropoietin (Epo) is the critical hormone for erythropoiesis. In adults, Epo is mainly produced by a subset of interstitial fibroblasts in the kidney, with minor amounts being produced in the liver and the brain. In this study, we used the immortalized renal interstitial fibroblast cell line FAIK F3-5 to investigate the ability of the bioactive sphingolipid sphingosine 1-phosphate (S1P) to stimulate Epo production and to reveal the mechanism involved. Stimulation of cells with exogenous S1P under normoxic conditions (21% O2) led to a dose-dependent increase in Epo mRNA and protein levels an

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Zhang, Gengqian, Sulei Xu, Yan Qian, and Pingnian He. "Sphingosine-1-phosphate prevents permeability increases via activation of endothelial sphingosine-1-phosphate receptor 1 in rat venules." American Journal of Physiology-Heart and Circulatory Physiology 299, no. 5 (2010): H1494—H1504. http://dx.doi.org/10.1152/ajpheart.00462.2010.

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Sphingosine-1-phosphate (S1P) has been demonstrated to enhance endothelial barrier function in vivo and in vitro. However, different S1P receptor subtypes have been indicated to play different or even opposing roles in the regulation of vascular barrier function. This study aims to differentiate the roles of endogenous endothelial S1P subtype receptors in the regulation of permeability in intact microvessels using specific receptor agonist and antagonists. Microvessel permeability was measured with hydraulic conductivity ( Lp) in individually perfused rat mesenteric venules. S1P-mediated chang

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Werth, Stephan, Helge Müller-Fielitz, and Walter Raasch. "Obesity-stimulated aldosterone release is not related to an S1P-dependent mechanism." Journal of Endocrinology 235, no. 3 (2017): 251–65. http://dx.doi.org/10.1530/joe-16-0550.

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Aldosterone has been identified as an important factor in obesity-associated hypertension. Here, we investigated whether sphingosine-1-phosphate (S1P), which has previously been linked to obesity, increases aldosterone release. S1P-induced aldosterone release was determined in NCI H295R cells in the presence of S1P receptor (S1PR) antagonists. In vivo release of S1P (100–300 µg/kgbw) was investigated in pithed, lean Sprague Dawley (SD) rats, diet-obese spontaneous hypertensive rats (SHRs), as well as in lean or obese Zucker rats. Aldosterone secretion was increased in NCI H295R cells by S1P, t

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Corvino, Angela, Ida Cerqua, Alessandra Lo Bianco, et al. "Antagonizing S1P3 Receptor with Cell-Penetrating Pepducins in Skeletal Muscle Fibrosis." International Journal of Molecular Sciences 22, no. 16 (2021): 8861. http://dx.doi.org/10.3390/ijms22168861.

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S1P is the final product of sphingolipid metabolism, which interacts with five widely expressed GPCRs (S1P1-5). Increasing numbers of studies have indicated the importance of S1P3 in various pathophysiological processes. Recently, we have identified a pepducin (compound KRX-725-II) acting as an S1P3 receptor antagonist. Here, aiming to optimize the activity and selectivity profile of the described compound, we have synthesized a series of derivatives in which Tyr, in position 4, has been substituted with several natural aromatic and unnatural aromatic and non-aromatic amino acids. All the comp

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Toebbe, JT, and Mary Beth Genter. "An Update on Sphingosine-1-Phosphate and Lysophosphatidic Acid Receptor Transcripts in Rodent Olfactory Mucosa." International Journal of Molecular Sciences 23, no. 8 (2022): 4343. http://dx.doi.org/10.3390/ijms23084343.

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Olfactory neurons connect the external environment and the brain, allowing the translocation of materials from the nasal cavity into the brain. The olfactory system is involved in SARS-CoV-2 infections; early in the pandemic declared in 2020, a loss of the sense of smell was found in many infected patients. Attention has also been focused on the role that the olfactory epithelium appears to play in the entry of the SARS-CoV-2 virus into the brain. Specifically, SARS-CoV-2 enters cells via the angiotensin-converting enzyme 2 protein (ACE2), which is found on supporting cells in the olfactory ep

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Godessart, Nuria, Sanam Mustafa, Vlad Dolgachev, et al. "The S1P1 receptor antagonist W146 induces lymphopenia in mice. Demonstration that functional antagonism of S1P1 is the mechanism of lymphopenia evoked by fingolimod-like compounds. (140.15)." Journal of Immunology 184, no. 1_Supplement (2010): 140.15. http://dx.doi.org/10.4049/jimmunol.184.supp.140.15.

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Abstract Agonists of sphingosine 1-phosphate receptor 1 (S1P1) are a novel class of immunosuppressants. S1P is the endogenous agonist of S1P1 and promotes lymphocyte egress from lymph nodes (LN) into blood. However, synthetic agonists like fingolimod prevent the egress, causing systemic lymphopenia. This apparent contradiction is explained by the concept of functional antagonism, according to which synthetic S1P1 agonists induce receptor internalization, making cells unresponsive to the endogenous S1P. If this mechanism is true, S1P1 antagonists should induce lymphopenia. We have fully charact

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Juarez, Julius G., Nadia Harun, Marilyn Thien, et al. "Sphingosine-1-phosphate facilitates trafficking of hematopoietic stem cells and their mobilization by CXCR4 antagonists in mice." Blood 119, no. 3 (2012): 707–16. http://dx.doi.org/10.1182/blood-2011-04-348904.

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Abstract CXCL12 and VCAM1 retain hematopoietic stem cells (HSCs) in the BM, but the factors mediating HSC egress from the BM to the blood are not known. The sphingosine-1-phosphate receptor 1 (S1P1) is expressed on HSCs, and S1P facilitates the egress of committed hematopoietic progenitors from the BM into the blood. In the present study, we show that both the S1P gradient between the BM and the blood and the expression of S1P1 are essential for optimal HSC mobilization by CXCR4 antagonists, including AMD3100, and for the trafficking of HSCs during steady-state hematopoiesis. We also demonstra

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Gandy, K. Alexa Orr, Daniel Canals, Mohamad Adada, et al. "Sphingosine 1-phosphate induces filopodia formation through S1PR2 activation of ERM proteins." Biochemical Journal 449, no. 3 (2013): 661–72. http://dx.doi.org/10.1042/bj20120213.

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Previously we demonstrated that the sphingolipids ceramide and S1P (sphingosine 1-phosphate) regulate phosphorylation of the ERM (ezrin/radixin/moesin) family of cytoskeletal proteins [Canals, Jenkins, Roddy, Hernande-Corbacho, Obeid and Hannun (2010) J. Biol. Chem. 285, 32476–3285]. In the present article, we show that exogenously applied or endogenously generated S1P (in a sphingosine kinase-dependent manner) results in significant increases in phosphorylation of ERM proteins as well as filopodia formation. Using phosphomimetic and non-phosphorylatable ezrin mutants, we show that the S1P-ind

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Kitada, Yoshihiko, Kazuo Kajita, Koichiro Taguchi, et al. "Blockade of Sphingosine 1-Phosphate Receptor 2 Signaling Attenuates High-Fat Diet-Induced Adipocyte Hypertrophy and Systemic Glucose Intolerance in Mice." Endocrinology 157, no. 5 (2016): 1839–51. http://dx.doi.org/10.1210/en.2015-1768.

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Abstract Sphingosine 1-phosphate (S1P) is known to regulate insulin resistance in hepatocytes, skeletal muscle cells, and pancreatic β-cells. Among its 5 cognate receptors (S1pr1–S1pr5), S1P seems to counteract insulin signaling and confer insulin resistance via S1pr2 in these cells. S1P may also regulate insulin resistance in adipocytes, but the S1pr subtype(s) involved remains unknown. Here, we investigated systemic glucose/insulin tolerance and phenotypes of epididymal adipocytes in high-fat diet (HFD)-fed wild-type and S1pr2-deficient (S1pr2−/−) mice. Adult S1pr2−/− mice displayed smaller

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Seitz, Gabriele, Sedat Yildirim, Andreas M. Boehmler, Lothar Kanz, and Robert Möhle. "Sphingosine 1-Phosphate (S1P) Induces Migration and ERK/MAP-Kinase-Dependent Proliferation in Chronic Lymphocytic Leukemia (B-CLL) Due to Expression of the G Protein-Coupled Receptors S1P1/4." Blood 106, no. 11 (2005): 4996. http://dx.doi.org/10.1182/blood.v106.11.4996.4996.

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Abstract Egress of lymphocytes from lymphoid organs into the circulation has been shown to depend on the presence of the lipid mediator sphingosine 1-phosphate (S1P) in the peripheral blood, and expression of corresponding S1P receptors (i.e., S1P1), that belong to the family of 7-transmembrane G protein-coupled receptors (GPCR). As circulating lymphocytic lymphoma cells are a hallmark of chronic lymphocytic leukemia, we analyzed expression of different S1P receptors and the effects of S1P on B-CLL cells. By qualitative and quantitative (TaqMan) RT-PCR, significant mRNA expression of S1P1 and

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Chumanevich, Alena, Piper Wedman, and Carole A. Oskeritzian. "Sphingosine-1-Phosphate/Sphingosine-1-Phosphate Receptor 2 Axis Can Promote Mouse and Human Primary Mast Cell Angiogenic Potential through Upregulation of Vascular Endothelial Growth Factor-A and Matrix Metalloproteinase-2." Mediators of Inflammation 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/1503206.

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Mast cells (MC) are present in most vascularized tissues around the vasculature likely exerting immunomodulatory functions. Endowed with diverse mediators, resident MC represent first-line fine-tuners of local microenvironment. Sphingosine-1-phosphate (S1P) functions as a pluripotent signaling sphingolipid metabolite in health and disease. S1P formation occurs at low levels in resting MC and is upregulated upon activation. Its export can result in type 2 S1P receptor- (S1PR2-) mediated stimulation of MC, further fueling inflammation. However, the role of S1PR2 ligation in proangiogenic vascula

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Zhu, Qing, Min Xia, Zhengchao Wang, Pin-Lan Li, and Ningjun Li. "A novel lipid natriuretic factor in the renal medulla: sphingosine-1-phosphate." American Journal of Physiology-Renal Physiology 301, no. 1 (2011): F35—F41. http://dx.doi.org/10.1152/ajprenal.00014.2011.

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Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid metabolite formed by phosphorylation of sphingosine. S1P has been indicated to play a significant role in the cardiovascular system. It has been shown that the enzymes for S1P metabolism are expressed in the kidneys. The present study characterized the expression of S1P receptors in the kidneys and determined the role of S1P in the control of renal hemodynamics and sodium excretion. Real-time RT-PCR analyses showed that S1P receptors S1P1, S1P2, and S1P3 were most abundantly expressed in the renal medulla. Immunohistochemistry revealed

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Niedernberg, Anke, Sorin Tunaru, Andree Blaukat, Bruce Harris, and Evi Kostenis. "Comparative Analysis of Functional Assays for Characterization of Agonist Ligands at G Protein-Coupled Receptors." Journal of Biomolecular Screening 8, no. 5 (2003): 500–510. http://dx.doi.org/10.1177/1087057103257555.

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A variety of functional assays are available for agonist or antagonist screening of G protein-coupled receptors (GPCRs), but it is a priori not predictable which assay is the most suitable to identify agonists or antagonists of GPCRs with therapeutic value in humans. More specifically, it is not known how a given set of GPCR agonists compares in different functional assays with respect to potency and efficacy and whether the level of the signaling cascade that is analyzed has any impact on the detection of agonistic responses. To address this question, the authors used the recently cloned huma

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Balthasar, Sonja, Johanna Samulin, Hanna Ahlgren, et al. "Sphingosine 1-phosphate receptor expression profile and regulation of migration in human thyroid cancer cells." Biochemical Journal 398, no. 3 (2006): 547–56. http://dx.doi.org/10.1042/bj20060299.

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S1P (sphingosine 1-phosphate) receptor expression and the effects of S1P on migration were studied in one papillary (NPA), two follicular (ML-1, WRO) and two anaplastic (FRO, ARO) thyroid cancer cell lines, as well as in human thyroid cells in primary culture. Additionally, the effects of S1P on proliferation, adhesion and calcium signalling were addressed in ML-1 and FRO cells. All cell types expressed multiple S1P receptors. S1P evoked intracellular calcium signalling in primary cultures, ML-1 cells and FRO cells. Neither proliferation nor migration was affected in primary cultures, whereas

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Alam, Shah, Sumaiya Yasmeen Afsar, Maya Anik Wolter, et al. "S1P Lyase Deficiency in the Brain Promotes Astrogliosis and NLRP3 Inflammasome Activation via Purinergic Signaling." Cells 12, no. 14 (2023): 1844. http://dx.doi.org/10.3390/cells12141844.

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Astrocytes are critical players in brain health and disease. Brain pathologies and lesions are usually accompanied by astroglial alterations known as reactive astrogliosis. Sphingosine 1-phosphate lyase (SGPL1) catalysis, the final step in sphingolipid catabolism, irreversibly cleaves its substrate sphingosine 1-phosphate (S1P). We have shown that neural ablation of SGPL1 causes accumulation of S1P and hence neuronal damage, cognitive deficits, as well as microglial activation. Moreover, the S1P/S1P-receptor signaling axis enhances ATP production in SGPL1-deficient astrocytes. Using immunohist

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Standoli, Sara, Sara Pecchioli, Daniel Tortolani, et al. "The TRPV1 Receptor Is Up-Regulated by Sphingosine 1-Phosphate and Is Implicated in the Anandamide-Dependent Regulation of Mitochondrial Activity in C2C12 Myoblasts." International Journal of Molecular Sciences 23, no. 19 (2022): 11103. http://dx.doi.org/10.3390/ijms231911103.

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The sphingosine 1-phosphate (S1P) and endocannabinoid (ECS) systems comprehend bioactive lipids widely involved in the regulation of similar biological processes. Interactions between S1P and ECS have not been so far investigated in skeletal muscle, where both systems are active. Here, we used murine C2C12 myoblasts to investigate the effects of S1P on ECS elements by qRT-PCR, Western blotting and UHPLC-MS. In addition, the modulation of the mitochondrial membrane potential (ΔΨm), by JC-1 and Mitotracker Red CMX-Ros fluorescent dyes, as well as levels of protein controlling mitochondrial funct

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Del Gaudio, Ilaria, Sebastian Hendrix, Christina Christoffersen, and Christian Wadsack. "Neonatal HDL Counteracts Placental Vascular Inflammation via S1P–S1PR1 Axis." International Journal of Molecular Sciences 21, no. 3 (2020): 789. http://dx.doi.org/10.3390/ijms21030789.

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Placental inflammation and dysfunction during pregnancy are associated with short- and long-term adverse outcomes for the offspring. However, the mechanisms of vascular protection at the feto-placental interface are still poorly investigated. The high-density lipoprotein (HDL) associated sphingosine-1-phosphate (S1P) has been described as a powerful anti-inflammatory complex. This study aimed to elucidate the role of cord blood-derived HDL (nHDL) in feto-placental endothelial dysfunction. Here, we report that the exposure of primary fetal placental arterial endothelial cell (fPAEC) to healthy

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Chen, Zhoumou, Timothy M. Doyle, Livio Luongo, et al. "Sphingosine-1-phosphate receptor 1 activation in astrocytes contributes to neuropathic pain." Proceedings of the National Academy of Sciences 116, no. 21 (2019): 10557–62. http://dx.doi.org/10.1073/pnas.1820466116.

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Neuropathic pain afflicts millions of individuals and represents a major health problem for which there is limited effective and safe therapy. Emerging literature links altered sphingolipid metabolism to nociceptive processing. However, the neuropharmacology of sphingolipid signaling in the central nervous system in the context of chronic pain remains largely unexplored and controversial. We now provide evidence that sphingosine-1-phosphate (S1P) generated in the dorsal horn of the spinal cord in response to nerve injury drives neuropathic pain by selectively activating the S1P receptor subtyp

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Tao, Rong, Holly E. Hoover, Norman Honbo, et al. "High-density lipoprotein determines adult mouse cardiomyocyte fate after hypoxia-reoxygenation through lipoprotein-associated sphingosine 1-phosphate." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 3 (2010): H1022—H1028. http://dx.doi.org/10.1152/ajpheart.00902.2009.

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The lipid mediator sphingosine 1-phosphate (S1P) confers survival benefits in cardiomyocytes and isolated hearts subjected to oxidative stress. High-density lipoprotein (HDL) is a major carrier of S1P in the serum, but whether HDL-associated S1P directly mediates survival in a preparation composed exclusively of cardiomyocytes has not been demonstrated. Accordingly, we tested the hypothesis that signal activation and survival during simulated ischemia-reperfusion injury in response to HDL require lipoprotein-associated S1P. As a model, we used adult mouse cardiomyocytes subjected to hypoxia-re

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Latif, Ahmed Abdel, Anush K. Karapetyan, Yuri Klyachkin, et al. "Novel Role for Bioactive Lipids in Mobilization of Bone Marrow Stem Cells During Myocardial Ischemia: Sphingosine-1 Phosphate (S1P) As Potential Therapeutic Target." Blood 120, no. 21 (2012): 1911. http://dx.doi.org/10.1182/blood.v120.21.1911.1911.

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Abstract Abstract 1911 Background: Bone marrow (BM) contains a variety of stem cells, including mobile pool of hematopoietic stem cells and non-hematopoietic stem cells and acute myocardial infarction (AMI) triggers mobilization of BM-derived stem cells (BMSCs) through poorly understood processes. Recently we have postulated a major role for bioactive lipids such as sphingosine-1 phosphate (S1P) in G-CSF- and AMD3100-induced mobilization of hematopoietic stem cells (HSCs) into peripheral blood (PB) (Leukemia 2010;24:976–85). Hypothesis: We hypothesized that S1P could also play a role in mobili

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Stockstill, Katherine, Timothy M. Doyle, Xisheng Yan, et al. "Dysregulation of sphingolipid metabolism contributes to bortezomib-induced neuropathic pain." Journal of Experimental Medicine 215, no. 5 (2018): 1301–13. http://dx.doi.org/10.1084/jem.20170584.

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The development of chemotherapy-induced painful peripheral neuropathy is a major dose-limiting side effect of many chemotherapeutics, including bortezomib, but the mechanisms remain poorly understood. We now report that bortezomib causes the dysregulation of de novo sphingolipid metabolism in the spinal cord dorsal horn to increase the levels of sphingosine-1-phosphate (S1P) receptor 1 (S1PR1) ligands, S1P and dihydro-S1P. Accordingly, genetic and pharmacological disruption of S1PR1 with multiple S1PR1 antagonists, including FTY720, blocked and reversed neuropathic pain. Mice with astrocyte-sp

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Schira-Heinen, Jessica, Luzhou Wang, Seda Akgün, et al. "Modulation of Specific Sphingosine-1-Phosphate Receptors Augments a Repair Mediating Schwann Cell Phenotype." International Journal of Molecular Sciences 23, no. 18 (2022): 10311. http://dx.doi.org/10.3390/ijms231810311.

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Transdifferentiation of Schwann cells is essential for functional peripheral nerve regeneration after injury. By activating a repair program, Schwann cells promote functional axonal regeneration and remyelination. However, chronic denervation, aging, metabolic diseases, or chronic inflammatory processes reduce the transdifferentiation capacity and thus diminish peripheral nerve repair. It was recently described that the sphingosine-1-phosphate receptor (S1PR) agonist Fingolimod enhances the Schwann cell repair phenotype by activation of dedifferentiation markers and concomitant release of trop

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Pernebay, A. N., A. M. Orynbaeva, B. K. Makhmutova, Sh B. Battakova, M. B. Otarbaeva, and M. A. Grigolashvili. "Current methods of diagnosis and treatment of neuropsychiatric disorders in systemic lupus erythematosus." Vestnik nevrologii, psihiatrii i nejrohirurgii (Bulletin of Neurology, Psychiatry and Neurosurgery), no. 10 (October 17, 2024): 1196–208. http://dx.doi.org/10.33920/med-01-2410-04.

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Neuropsychiatric systemic lupus erythematosus (NPSLE) is a severe complication of systemic lupus erythematosus (SLE), characterized by damage to the nervous system. The article discusses the pathogenesis, clinical manifestations, laboratory and instrumental diagnostics, as well as modern and promising methods of treating NPSLE. Both immunoinflammatory (autoantibodies, cytokines) and ischemic (thrombosis, vasculitis) mechanisms are involved in the NPSLE pathogenesis. The clinical picture is varied and includes cognitive impairment, headache, seizures, psychosis, and other neurological and psych

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Landeen, Lee K., Dorothy A. Dederko, Colleen S. Kondo, et al. "Mechanisms of the negative inotropic effects of sphingosine-1-phosphate on adult mouse ventricular myocytes." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 2 (2008): H736—H749. http://dx.doi.org/10.1152/ajpheart.00316.2007.

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Sphingosine-1-phosphate (S1P) induces a transient bradycardia in mammalian hearts through activation of an inwardly rectifying K+ current ( IKACh) in the atrium that shortens action potential duration (APD) in the atrium. We have investigated probable mechanisms and receptor-subtype specificity for S1P-induced negative inotropy in isolated adult mouse ventricular myocytes. Activation of S1P receptors by S1P (100 nM) reduced cell shortening by ∼25% (vs. untreated controls) in field-stimulated myocytes. S1P1 was shown to be involved by using the S1P1-selective agonist SEW2871 on myocytes isolate

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Stepanovska Tanturovska, Bisera, Aleksandra Zivkovic, Faik Imeri, et al. "ST-2191, an Anellated Bismorpholino Derivative of Oxy-Fingolimod, Shows Selective S1P1 Agonist and Functional Antagonist Potency In Vitro and In Vivo." Molecules 26, no. 17 (2021): 5134. http://dx.doi.org/10.3390/molecules26175134.

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Sphingosine 1-phosphate (S1P) is an extensively studied signaling molecule that contributes to cell proliferation, survival, migration and other functions through binding to specific S1P receptors. The cycle of S1P1 internalization upon S1P binding and recycling to the cell surface when local S1P concentrations are low drives T cell trafficking. S1P1 modulators, such as fingolimod, disrupt this recycling by inducing persistent S1P1 internalization and receptor degradation, which results in blocked egress of T cells from the secondary lymphoid tissues. The approval of these compounds for the tr

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Hla, Timothy, Sylvain Galvani, Shahin Rafii, and Ralph Nachman. "S1P and the birth of platelets." Journal of Experimental Medicine 209, no. 12 (2012): 2137–40. http://dx.doi.org/10.1084/jem.20122284.

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Recent work has highlighted the multitude of biological functions of sphingosine 1-phosphate (S1P), which include roles in hematopoietic cell trafficking, organization of immune organs, vascular development, and neuroinflammation. Indeed, a functional antagonist of S1P1 receptor, FTY720/Gilenya, has entered the clinic as a novel therapeutic for multiple sclerosis. In this issue of the JEM, Zhang et al. highlight yet another function of this lipid mediator: thrombopoiesis. The S1P1 receptor is required for the growth of proplatelet strings in the bloodstream and the shedding of platelets into t

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Luo, Dongdong, Zhikun Guo, Xuecui Zhao, et al. "Novel 5-fluorouracil sensitizers for colorectal cancer therapy: Design and synthesis of S1P receptor 2 (S1PR2) antagonists." European Journal of Medicinal Chemistry 227 (January 2022): 113923. http://dx.doi.org/10.1016/j.ejmech.2021.113923.

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Maceyka, Michael, Sergio E. Alvarez, Sheldon Milstien, and Sarah Spiegel. "Filamin A Links Sphingosine Kinase 1 and Sphingosine-1-Phosphate Receptor 1 at Lamellipodia To Orchestrate Cell Migration." Molecular and Cellular Biology 28, no. 18 (2008): 5687–97. http://dx.doi.org/10.1128/mcb.00465-08.

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ABSTRACT Sphingosine kinase 1 (SphK1) catalyzes the phosphorylation of sphingosine to produce the potent lipid mediator sphingosine-1-phosphate (S1P), which plays a critical role in cell motility via its cell surface receptors. Here, we have identified filamin A (FLNa), an actin-cross-linking protein involved in cell movement, as a bona fide SphK1-interacting protein. Heregulin stimulated SphK1 activity only in FLNa-expressing A7 melanoma cells but not in FLNa-deficient cells and induced its translocation and colocalization with FLNa at lamellipodia. SphK1 was required for heregulin-induced mi

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Lee, Chi-Ho, and Ji Woong Choi. "S1P/S1P2 Signaling Axis Regulates Both NLRP3 Upregulation and NLRP3 Inflammasome Activation in Macrophages Primed with Lipopolysaccharide." Antioxidants 10, no. 11 (2021): 1706. http://dx.doi.org/10.3390/antiox10111706.

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The activation of NLRP3 inflammasome is a key factor for various inflammatory diseases. Here, we provide experimental evidence supporting the regulatory role of sphingosine-1-phosphate (S1P) in NLRP3 inflammasome activation in mouse bone-marrow-derived macrophages (BMDMs), along with the S1P receptor subtype involved and underlying regulatory mechanisms. During the priming stage, S1P induced NLRP3 upregulation in BMDMs only when primed with lipopolysaccharide (LPS). In this event, S1P2, but not S1P1, was involved based on the attenuated NLRP3 upregulation with JTE013 (S1P2 antagonist) or S1P2

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Lee, Jen-Fu, Sharon Gordon, Rosendo Estrada, et al. "Balance of S1P1and S1P2signaling regulates peripheral microvascular permeability in rat cremaster muscle vasculature." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 1 (2009): H33—H42. http://dx.doi.org/10.1152/ajpheart.00097.2008.

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Sphingosine-1-phosphate (S1P) regulates various molecular and cellular events in cultured endothelial cells, such as cytoskeletal restructuring, cell-extracellular matrix interactions, and intercellular junction interactions. We utilized the venular leakage model of the cremaster muscle vascular bed in Sprague-Dawley rats to investigate the role of S1P signaling in regulation of microvascular permeability. S1P signaling is mediated by the S1P family of G protein-coupled receptors (S1P1-5receptors). S1P1and S1P2receptors, which transduce stimulatory and inhibitory signaling, respectively, are e

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Zhang, Yujin, Shushan Zhao, Hongyu Wu, et al. "Sphingosine 1-Phosphate (S1P)/S1P Receptor 1 Pathway Has an Essential Role for Sickle Cell Disease." Blood 124, no. 21 (2014): 4063. http://dx.doi.org/10.1182/blood.v124.21.4063.4063.

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Abstract Sickle cell disease (SCD) is a devastating hemolytic genetic disorder associated with high morbidity and mortality. In order to understand the pathogenesis of this disease, we have conducted non-biased metabolomic screening and found that circulating sphingosine-1-phosphate (S1P) was significantly elevated in mice and patients with SCD. S1P is an important bioactive lipid signaling molecule known to regulate inflammation. Our previous study demonstrated that reduced S1P level in plasma and erythrocytes by treatment with sphingosine kinase 1 (SPHK1) inhibitor, PF-543, significantly dec

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Yoon, Chang Min, Bok Sil Hong, Hyung Geun Moon, et al. "Sphingosine-1-phosphate promotes lymphangiogenesis by stimulating S1P1/Gi/PLC/Ca2+ signaling pathways." Blood 112, no. 4 (2008): 1129–38. http://dx.doi.org/10.1182/blood-2007-11-125203.

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Abstract The lymphatic system plays pivotal roles in mediating tissue fluid homeostasis and immunity, and excessive lymphatic vessel formation is implicated in many pathological conditions, which include inflammation and tumor metastasis. However, the molecular mechanisms that regulate lymphatic vessel formation remain poorly characterized. Sphingosine-1-phosphate (S1P) is a potent bioactive lipid that is implicated in a variety of biologic processes such as inflammatory responses and angiogenesis. Here, we first report that S1P acts as a lymphangiogenic mediator. S1P induced migration, capill

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Koch, Alexander, Manuel Jäger, Anja Völzke, et al. "Downregulation of sphingosine 1-phosphate (S1P) receptor 1 by dexamethasone inhibits S1P-induced mesangial cell migration." Biological Chemistry 396, no. 6-7 (2015): 803–12. http://dx.doi.org/10.1515/hsz-2014-0288.

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Abstract Sphingosine 1-phosphate (S1P) is generated by sphingosine kinase (SK)-1 and -2 and acts mainly as an extracellular ligand at five specific receptors, denoted S1P1–5. After activation, S1P receptors regulate important processes in the progression of renal diseases, such as mesangial cell migration and survival. Previously, we showed that dexamethasone enhances SK-1 activity and S1P formation, which protected mesangial cells from stress-induced apoptosis. Here we demonstrate that dexamethasone treatment lowered S1P1 mRNA and protein expression levels in rat mesangial cells. This effect

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El-Shewy, Hesham M., Mimi Sohn, Parker Wilson, et al. "Low-Density Lipoprotein Induced Expression of Connective Tissue Growth Factor via Transactivation of Sphingosine 1-Phosphate Receptors in Mesangial Cells." Molecular Endocrinology 26, no. 5 (2012): 833–45. http://dx.doi.org/10.1210/me.2011-1261.

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Abstract The pro-fibrotic connective tissue growth factor (CTGF) has been linked to the development and progression of diabetic vascular and renal disease. We recently reported that low-density lipoproteins (LDL) induced expression of CTGF in aortic endothelial cells. However, the molecular mechanisms are not fully defined. Here, we have studied the mechanism by which LDL regulates CTGF expression in renal mesangial cells. In these cells, treatment with pertussis toxin abolished LDL-stimulated activation of ERK1/2 and c-Jun N-terminal kinase (JNK), indicating the involvement of heterotrimeric

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&NA;. "INTERNALIZATION OF THE S1P-1 RECEPTOR IS MEDIATED BY AGONISTS AND NOT BY ANTAGONISTS BUT DOES NOT REQUIRE INTRACELLULAR SIGNALING." Transplantation 82, Suppl 2 (2006): 426–27. http://dx.doi.org/10.1097/00007890-200607152-01067.

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Pelz, Andreas, Hanne Schaffert, Radharani Diallo, Falk Hiepe, Andreas Meisel, and Siegfried Kohler. "S1P receptor antagonists fingolimod and siponimod do not improve the outcome of experimental autoimmune myasthenia gravis mice after disease onset." European Journal of Immunology 48, no. 3 (2017): 498–508. http://dx.doi.org/10.1002/eji.201747187.

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Damirin, Alatangaole, Hideaki Tomura, Mayumi Komachi, et al. "Role of lipoprotein-associated lysophospholipids in migratory activity of coronary artery smooth muscle cells." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 5 (2007): H2513—H2522. http://dx.doi.org/10.1152/ajpheart.00865.2006.

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The migration of vascular smooth muscle cells (SMCs) is a hallmark of the pathogenesis of atherosclerosis and restenosis after angioplasty. Plasma low-density lipoprotein (LDL), but not high-density lipoprotein (HDL), induced the migration of human coronary artery SMCs (CASMCs). Among bioactive lipids postulated to be present in LDL, lysophosphatidic acid (LPA) appreciably mimicked the LDL action. In fact, the LDL-induced migration was markedly inhibited by pertussis toxin, an LPA receptor antagonist Ki-16425, and a small interfering RNA (siRNA) targeted for LPA1 receptors. Moreover, LDL conta

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Germinario, Elena, Samantha Peron, Luana Toniolo, et al. "S1P2 receptor promotes mouse skeletal muscle regeneration." Journal of Applied Physiology 113, no. 5 (2012): 707–13. http://dx.doi.org/10.1152/japplphysiol.00300.2012.

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Sphingosine 1-phosphate is a bioactive lipid that modulates skeletal muscle growth through its interaction with specific receptors localized in the cell membrane of muscle fibers and satellite cells. This study analyzes the role of S1P2 receptor during in vivo regeneration of soleus muscle in two models of S1P2 deficiency: the S1P2-null mouse and wild-type mice systemically treated with the S1P2 receptor antagonist JTE-013. To stimulate regeneration, muscle degeneration was induced by injecting into soleus muscle the myotoxic drug notexin. Both ablation of S1P2 receptor and its functional inac

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Igawa, Satomi, Jae Eun Choi, Zhenping Wang, et al. "Sphingosine 1-phosphate is a harbinger of S. aureus invasion and activates host defense in epithelial barriers." Journal of Immunology 202, no. 1_Supplement (2019): 126.30. http://dx.doi.org/10.4049/jimmunol.202.supp.126.30.

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Abstract Background Sphingosine 1-phosphate (S1P) is a bioactive lipid mediator generated in the skin when cell membrane or barrier components are damaged. S1P regulates diverse cell activities via S1P receptors (S1PR). Keratinocytes express S1PR1–5. Although it is known that S1PRs control keratinocyte differentiation, apoptosis and wound healing, S1PR functions in keratinocyte infections are not fully elucidated. We hypothesized that S1P and S1PR-axis in keratinocytes works as a biosensor for bacterial invasion. Methods The expression of S1PRs were studied by immunofluorescence and qPCR. Cyto

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Cohan, Stanley, Elisabeth Lucassen, Kyle Smoot, Justine Brink, and Chiayi Chen. "Sphingosine-1-Phosphate: Its Pharmacological Regulation and the Treatment of Multiple Sclerosis: A Review Article." Biomedicines 8, no. 7 (2020): 227. http://dx.doi.org/10.3390/biomedicines8070227.

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Sphingosine-1-phosphate (S1P), via its G-protein-coupled receptors, is a signaling molecule with important regulatory properties on numerous, widely varied cell types. Five S1P receptors (S1PR1-5) have been identified, each with effects determined by their unique G-protein-driven downstream pathways. The discovery that lymphocyte egress from peripheral lymphoid organs is promoted by S1P via S1PR-1 stimulation led to the development of pharmacological agents which are S1PR antagonists. These agents promote lymphocyte sequestration and reduce lymphocyte-driven inflammatory damage of the central

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Whetzel, Angela M., David T. Bolick, and Catherine C. Hedrick. "Sphingosine-1-phosphate inhibits high glucose-mediated ERK1/2 action in endothelium through induction of MAP kinase phosphatase-3." American Journal of Physiology-Cell Physiology 296, no. 2 (2009): C339—C345. http://dx.doi.org/10.1152/ajpcell.00293.2008.

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Endothelial activation is a key early event in vascular complications of Type 1 diabetes. The nonobese diabetic (NOD) mouse is a well-characterized model of Type 1 diabetes. We previously reported that Type 1 diabetic NOD mice have increased endothelial activation, with increased production of monocyte chemoattractant protein (MCP)-1 and IL-6, and a 30% increase of surface VCAM-1 expression leading to a fourfold increase in monocyte adhesion to the endothelium. Sphingosine-1-phosphate (S1P) prevents monocyte:endothelial interactions in these diabetic NOD mice. Incubation of diabetic NOD endoth

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Schwalm, Stephanie, Tankica Maneva Timcheva, Iuliia Filipenko, et al. "Sphingosine kinase 2 deficiency increases proliferation and migration of renal mouse mesangial cells and fibroblasts." Biological Chemistry 396, no. 6-7 (2015): 813–25. http://dx.doi.org/10.1515/hsz-2014-0289.

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Abstract Both of the sphingosine kinase (SK) subtypes SK-1 and SK-2 catalyze the production of the bioactive lipid molecule sphingosine 1-phosphate (S1P). However, the subtype-specific cellular functions are largely unknown. In this study, we investigated the cellular function of SK-2 in primary mouse renal mesangial cells (mMC) and embryonic fibroblasts (MEF) from wild-type C57BL/6 or SK-2 knockout (SK2ko) mice. We found that SK2ko cells displayed a significantly higher proliferative and migratory activity when compared to wild-type cells, with concomitant increased cellular activities of the

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Laroche, Fabrice J. F., Sheng Li, Ning Shen, et al. "S1P1 Threonine 236 Phosphorylation Mediates the Invasiveness of Triple-Negative Breast Cancer and Sensitivity to FTY720." Cells 12, no. 7 (2023): 980. http://dx.doi.org/10.3390/cells12070980.

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Hyperactive sphingosine 1-phosphate (S1P) signaling is associated with a poor prognosis of triple-negative breast cancer (TNBC). Despite recent evidence that links the S1P receptor 1 (S1P1) to TNBC cell survival, its role in TNBC invasion and the underlying mechanisms remain elusive. Combining analyses of human TNBC cells with zebrafish xenografts, we found that phosphorylation of S1P receptor 1 (S1P1) at threonine 236 (T236) is critical for TNBC dissemination. Compared to luminal breast cancer cells, TNBC cells exhibit a significant increase of phospho-S1P1 T236 but not the total S1P1 levels.

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Kalhori, Veronica, Melissa Magnusson, Muhammad Yasir Asghar, Ilari Pulli, and Kid Törnquist. "FTY720 (Fingolimod) attenuates basal and sphingosine-1-phosphate-evoked thyroid cancer cell invasion." Endocrine-Related Cancer 23, no. 5 (2016): 457–68. http://dx.doi.org/10.1530/erc-16-0050.

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The bioactive lipid sphingosine-1-phosphate (S1P) is a potent inducer of ML-1 thyroid cancer cell migration and invasion. It evokes migration and invasion by activating S1P receptor 1 and 3 (S1P1,3) and downstream signaling intermediates as well as through cross-communication with vascular endothelial growth factor receptor 2 (VEGFR2). However, very little is known about the role of S1P receptors in thyroid cancer. Furthermore, the currently used treatments for thyroid cancer have proven to be rather unsuccessful. Thus, due to the insufficiency of the available treatments for thyroid cancer, n

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Oskeritzian, Carole A., Megan M. Price, Nitai C. Hait, et al. "Essential roles of sphingosine-1–phosphate receptor 2 in human mast cell activation, anaphylaxis, and pulmonary edema." Journal of Experimental Medicine 207, no. 3 (2010): 465–74. http://dx.doi.org/10.1084/jem.20091513.

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Systemic exacerbation of allergic responses, in which mast cells play a critical role, results in life-threatening anaphylactic shock. Sphingosine-1–phosphate (S1P), a ligand for a family of G protein–coupled receptors, is a new addition to the repertoire of bioactive lipids secreted by activated mast cells. Yet little is known of its role in human mast cell functions and in anaphylaxis. We show that S1P2 receptors play a critical role in regulating human mast cell functions, including degranulation and cytokine and chemokine release. Immunoglobulin E–triggered anaphylactic responses, includin

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Curry, F. E., J. F. Clark, and R. H. Adamson. "Erythrocyte-derived sphingosine-1-phosphate stabilizes basal hydraulic conductivity and solute permeability in rat microvessels." American Journal of Physiology-Heart and Circulatory Physiology 303, no. 7 (2012): H825—H834. http://dx.doi.org/10.1152/ajpheart.00181.2012.

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Exogenous sphingosine-1-phosphate (S1P), a lipid mediator in blood, attenuates acute microvascular permeability increases via receptor S1P1 to stabilize the endothelium. To evaluate the contribution of erythrocytes as an endogenous source of S1P to the regulation of basal permeability, we measured permeability coefficients in intact individually perfused venular microvessels of rat mesentery. This strategy also enabled the contributions of other endogenous S1P sources to be evaluated. Apparent permeability coefficients ( PS) to albumin and α-lactalbumin and the hydraulic conductivity of mesent

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dela Paz, Nathaniel G., Benoît Melchior та John A. Frangos. "Shear stress induces Gαq/11 activation independently of G protein-coupled receptor activation in endothelial cells". American Journal of Physiology-Cell Physiology 312, № 4 (2017): C428—C437. http://dx.doi.org/10.1152/ajpcell.00148.2016.

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Mechanochemical signal transduction occurs when mechanical forces, such as fluid shear stress, are converted into biochemical responses within the cell. The molecular mechanisms by which endothelial cells (ECs) sense/transduce shear stress into biological signals, including the nature of the mechanosensor, are still unclear. G proteins and G protein-coupled receptors (GPCRs) have been postulated independently to mediate mechanotransduction. In this study, we used in situ proximity ligation assay (PLA) to investigate the role of a specific GPCR/Gαq/11 pair in EC shear stress-induced mechanotran

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