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sphingosine Kinase-1/sphingosine 1-phosphate pathway in diabetic nephropathy

Chinese Medical Journal 2014年第16期127卷 3004-3010页

作者： Deng Yanhui Lan Tian Huang Juan Huang Heqing Department of Pharmacy the Third Affiliated Hospital of Southern Medical University Guangzhou Guangdong 510630 China Institute of Vascular Biology Guangdong Pharmaceutical UniversityGuangzhou Guangdong 510006 China Laboratory of Pharmacology and Toxicology School of Pharmaceutical Sciences Sun Yat-sen University GuangzhouGuangdong 510006 China

Objective Diabetic nephropathy （DN） is the major cause of end-stage renal disease worldwide and its prevalence continues to increase.Currently,therapies for DN provide only partial renoprotection; hence new targets for therapeutic intervention need to be identified.In this review,we summarized the new target,sphingosine kinase-1/sphingosine 1-phosphate （SphK1/S1P） pathway,explored its potential therapeutic role in the prevention and treatment of DN.Data sources Most relevant articles were mainly identified by searching PubMed in English.Study selection Mainly original articles and critical review articles by major pioneer investigators in this field were selected to be reviewed.Results SphK1/S1P pathway can be activated by hyperglycemia,advanced glycation end products,and many proinflammatory cytokines,which leads to fibronectin,transforming growth factor-31 up-regulation and AP-1 activation.And then it could promote glomerular mesangial cells proliferation and extracellular matrix accumulation,mediating the initiation and progression of diabetic renal fibrosis.Conclusions SphK1/S1P pathway is closely correlated with the pathogenesis of DN.The results suggest that SphK1/ S1P pathway as a new target for clinically improving DN in future is of great prospect.

关键词： diabetic nephropathy sphingosine kinase-1 sphingosine 1-phosphate fibrosis transforming growth factor-β extracellular matrix

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sphingosine 1-phosphate in inflammation

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Journal of Clinical and Nursing Research 2020年第6期4卷 20-22页

作者： Lijuan Li Lixia An Lifang Li Yongjuan Zhao College of Information Shanxi Agricultural UniversityTaiyuan 030800China

Sphingolipids are formed via the metabolism of sphingomyelin,aconstituent of the plasma membrane.or by denovosynthesis.Enzymatic pathways result in the formation of sevenal different lipid meiators,which are knowm to bave important roles in many elllar proceses.imcluding polfeatioe,apoptosis and migation Several studies nDowr suggest that these shingolipid mediators,inchding cenamide,ceramside i-pbosphate and sphingosine 1-pbosphate(SIP).are likely to have a integral role in infamation.This can involve,for example activation of po-inammatory transcription factors in different cell types and indiuction of cyloxygenase-2.leading t如o productio of pro-inamatory prostaglandins.The mode of action of each sphingolipid is different.Increased ceramide production leads to the formation of ceramide-rich areas of the membnane.which may assemble sigalling compleses,whereas SIP acts via b-affnity G-protein-coupled SIP receptors on the plasma membrane.Recent studies bave demonstated that in vitro efects of sphingolipids o infammation can translate into in vivo models.This review will higblight the areas of research where spbingolipids ae involved in infamomation and the mecharisms of acion of each mediator.In adirion,the therpeutic poternial of dinugs that alter sphingolipid actions mill be exmined with reference to disease states,such as asthma and infammatary bowel disease,which invove importanot ifmaxmsutory components.A signifcant body of research now indicates that sphingolipids ure intimately inolved in the infammatory process and recent studies have demonstated that these lipids.together with associated enzymes and receptors,can provide effective drug targets for the treatment of pathological inflammation.

关键词： Infammation Sphingolipids sphingosine 1-phosphate

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sphingosine 1-phosphate-elevated calcium inactivates NPR2 that is required for oocyte meiotic resumption in mouse

Sphingosine 1-phosphate-elevated calcium inactivates NPR2 th...

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中国生理学会生殖科学专业委员会—中国动物学会生殖生物学...

作者： Xiaoqiong Hao Feifei Yuan Jing Yang Yu Zhang Xiaoting Xu You-Qiang Su Meijia Zhang China Agricultural University

In preovulatory ovarian follicles,oocyte is maintained in meiotic prophase arrest by natriuretic peptide type C(NPPC) and its receptor guanylylcyclase-linked natriuretic peptide receptor 2(NPR2).LH-activated epidermal growth factor(EGF) receptor signaling increases calcium levels of cumulus cells resulting in the inactivation of NPR2 that promotes resumption of meiotic.Here,we investigated the regulatory mechanism of LH-EGF receptor signaling-elevated calcium levels in cumulus cells.Cumulus cell-oocyte complexes(COCs) were cultured in the present of NPPC.In this culture system,EGF could increase intracellular calcium concentration of cumulus cells to stimulate oocyte meiotic resumption.However,the inhibition of sphingosine kinase(SphK) by SKI-II completely blocked the EGF-induced calcium elevation and oocyte maturation.SphK catalyzes the phosphorylation of sphingosine to generate sphingosine 1-phosphate(S1 P),which can induce calcium release from the endoplasmic reticulum(ER).LH-EGF receptor signaling elevated S1 P concentration of COCs.S1 P elevated calcium levels of cumulus cell,and decreased the binding affinity of NPR2 for NPPC,resulting in oocyte meiotic resumption.Further study indicated that 50μM U0126 could block EGF-induced increase of S1 P levels,suggesting that EGF increased S1 P levels through the activation of MAPK3/1.After that,we studied the SphK1;SphK2;FshR-cre mice to identify the effect of SphK1 and SphK2 on oocyte meiotic resumption of mouse.Oocyte maturation was delayed after injection of human chorionic gonadotropin(hCG) in these mice.In vitro,EGF could also not promote meiotic resumption of COCs collected from these mice.Furthermore,the number of eggs ovulated by each mouse decreased 50%compared with the control.The breeding assay indicated that the reproductive performance significantly decrease in SphK1;SphK2;FshR-cre mice.S1 P levels are also mediated by reversible dephosphoryltion with S1 P phosphatases(SGPP,also known as SPP) and irreversible degradation with sphingosine phosphate lyase

关键词： sphingosine 1-phosphate SphK SGPLl NPR2 Calcium Oocyte

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sphingosine signaling and atherogenesis

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Acta Pharmacologica Sinica 2004年第7期25卷 3-8页

作者： Jacob HANSEN-SCHWARTZ,Lars EDVINSSON Department of Clinical Experimental Research Glostrup University Hospital Glostrup Denmark Division of Experimental Vascular Research Institute of Medicine Lund University Sweden

sphingosine-1-phosphate (S1P) has diverse biological functions acting inside cells as a second messenger toregulate cell proliferation and survival, and extracellularly, as a ligand for a group of G protein-coupled receptors(GPCRs) named the endothelial differentiation gene (EDG) family. Five closely related GPCRs of EDG family(EDG1, EDG3, EDG5, EDG6, and EDG8) have recently been identified as high-affinity S1P receptors. Thesereceptors are coupled via Gi, Gq, G12/13, and Rho. The signaling pathways are linked to vascular cell migration,proliferation, apoptosis, intracellular Ca2+ mobilization, and expression of adhesion molecules. The formation of anatherosclerotic lesion occurs through activation of cellular events that include monocyte adhesion to the endothe-lium and vascular smooth muscle cell (VSMC) migration and proliferation. Thus, S1P signaling may play animportant role in the pathogenesis of atherosclerotic vascular disease. This review highlights S1P signalling invascular cells and its involvement in the formation of atherosclerotic lesions.

关键词： sphingosine 1-phosphate sphingosine kinase sphingosine-1-phosphate receptors endothelium myocardium smooth muscle arteriosclerosis

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Cross-Talk between Extracellular S1P/S1P2 and P42/44 MAPK in bcr/abl Positive Chronic Myeloid Leukemia Cells

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Chinese Journal of Cancer Research 2009年第1期21卷 20-27页

作者： Yin Xu Fei-qun Zheng Qun-wei Zhang Yang Liu Hai-feng Duan Chun-ping Cui Bin Wu Yi-de Qin Deparment of Biochemistry and Molecular Biology Anhui Medical University Hefei 230032 China Department of Experimental Hematology Beijing Institute of Radiation Medicine Beijing 100850 China Key Laboratory of Carcinogenesis and Translational Research （Ministry of Education） Department of lnterventional Therapy Peking University School of Oncology Beijing Cancer Hospital ＆ Institute Beijing 100142 China

Objective： BCR/ABL oncoprotein-expression is associated with uncontrolled cell growth. sphingosine kinase 1 （SPK1） regulates the production of sphingosine 1-phosphate （S1P）, a key lipid signal molecular in cell proliferation and survival. The objective of this study was to elucidate the roles of S1P and its receptors in bcr/abl positive chronic myeloid leukemia （CML） cells. Methods： The expressions of SIP receptors： S1P1, S1P2 and S1P3 in CML cells were detected by RT-PCR. SPK1 expression, activity and extracellular S1P were determined in ECV304 and HL-60 cells which were transfected with bcr/abl gene. To elucidate the relationship between the BCR/ABL, ERK/MAPK （extracellular signal-regulated kinase/mitogen-activated protein kinase）, SPK/S 1P and S 1P/S 1 P2 signal pathways, bcr/abl positive CML cell line K562 was treated with STI571, PD98059, N,N-dimethyl sphingosine （DMS） and JTE-013. Results： Retrovirus-mediated overexpression of bcr/abl gene in ECV304 and HL-60 cells resulted in upregulation of the expression, activity of SPK1 and increase of the secretion of SIP, whereas treatment of STI571 and PD98059 decreased the BCR/ABL-induced S1P secretion. Treatment of DMS reduced S1P secretion and P42/44MAPK phosphorylation. S1P2-selective antagonist JTE-013 could also decrease P42/44MAPK phosphorylation. Conclusion： These results suggest that BCR/ABL up-regulates extracellular sphingosine 1-phosphate through sphingosine kinase 1 and there is cross-talk between SPK1/S1P/S1P2 and P42/44MAPK in bcr/abl positive CML cells.

关键词： sphingosine kinase sphingosine 1-phosphate CML Extracellular signal-regulated kinase/mitogen-activated protein kinase Cross-talk

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Bioactive lipids and cancer metastasis to bone

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Journal of Cancer Metastasis and Treatment 2021年第1期7卷 604-627页

作者： Lou Saier Hira Niazi Leyre Brizuela Bodo Levkau Olivier Peyruchaud INSERM Unit 1033LYOSLyon 69372France UniversitéClaude Bernard Lyon 1 Lyon 69372France INSERM Unit 970 Paris Cardiovascular Research CentreParis 75015France Universitéde Paris Paris 75015France CNRS UMR 5246 INSA LyonInstitut de Chimie et Biochimie Moléculaires et Supramoléculaires(ICBMS)Lyon 69622France Institute for Molecular Medicine III and University Hospital Düsseldorf DüsseldorfHeinrich Heine UniversitätDüsseldorf 40225Germany

Bioactive lipids constitute a large family of molecules considered as inflammatory mediators.Among them,lysophosphatidic acid(LPA),sphingosine 1-phosphate(S1P),and eicosanoids(prostanoids such as PGE2 and leukotrienes such as LTB4,LTC4,and LTD4)play a central role in the pathophysiology of several inflammatory diseases.However,it has long been known that these bioactive lipids are also involved in cancer,mainly because of their ability to control the pro-inflammatory microenvironment of tumors as well as their ability to act directly on tumor cells promoting cell proliferation,migration,and survival.Recently,there has been increased interest in determining how these lipid mediators orchestrate tumor development and metastasis.Bone metastases result from a complex dialogue between tumor cells and bone cells.Recent findings demonstrate that all these bioactive lipids can profoundly affect bone metabolism by acting positively or negatively on both osteoblasts and osteoclasts.This review gives an overview of previous findings demonstrating direct involvement of LPA,S1P,and PGE2 in bone metastasis.This review also emphasizes the recent findings that characterize the activity of these bioactive lipids directly on bone cells and how these activities could be integrated into the complex molecular mechanisms leading to bone metastasis formation and progression.

关键词： Lysophosphatidic acid sphingosine 1-phosphate eicosanoids prostaglandins leukotrienes cancer bone cells

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S1P对骨髓间质干细胞向纤维化肝脏迁移归巢的作用

S1P对骨髓间质干细胞向纤维化肝脏迁移归巢的作用

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中国细胞生物学学会第九次会员代表大会暨青年学术大会

作者：李长勇孔雅娴王宏姜向明俞豪刘欣杨琳杨荟敏李丽英首都医科大学

肝纤维化的病理特征是细胞外基质(ECM)在肝内过量沉积,而肝脏肌成纤维细胞(hMF)是分泌 ECM 的主要细胞。hMF 的来源存在异源性,而其中之一的骨髓源性的研究倍受关注。本课题拟结合体内和体外研究方法,证实在肝纤维化发生过程中骨髓间质... 详细信息

肝纤维化的病理特征是细胞外基质(ECM)在肝内过量沉积,而肝脏肌成纤维细胞(hMF)是分泌 ECM 的主要细胞。hMF 的来源存在异源性,而其中之一的骨髓源性的研究倍受关注。本课题拟结合体内和体外研究方法,证实在肝纤维化发生过程中骨髓间质干细胞(MSCs)可向肝脏迁移并分化为 hMF,并以磷酸鞘氨醇(S1P)为靶分子,探讨其介导 MSCs 向纤维化肝脏归巢的作用。

关键词： sphingosine 1-phosphate 骨髓间质干细胞细胞移植肝纤维化细胞迁移

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