• Natural Product Sciences
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• v.9 no.3
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• pp.117-142
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• 2003

The sphingolipids isolated from marine organisms and their biological activities have been reviewed.

• BMB Reports
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• v.53 no.1
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• pp.28-34
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• 2020

Sphingolipids are ubiquitous building blocks of eukaryotic cell membranes that function as signaling molecules for regulating a diverse range of cellular processes, including cell proliferation, growth, survival, immune-cell trafficking, vascular and epithelial integrity, and inflammation. Recently, several studies have highlighted the pivotal role of sphingolipids in neuroinflammatory regulation. Sphingolipids have multiple functions, including induction of the expression of various inflammatory mediators and regulation of neuroinflammation by directly effecting the cells of the central nervous system. Accumulating evidence points to sphingolipid engagement in neuroinflammatory disorders, including Alzheimer's and Parkinson's diseases. Abnormal sphingolipid alterations, which involves an increase in ceramide and a decrease in sphingosine kinase, are observed during neuroinflammatory disease. These trends are observed early during disease development, and thus highlight the potential of sphingolipids as a new therapeutic and diagnostic target for neuroinflammatory diseases.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.213.1-213.1
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• 2003

Sphingolipids and their metabolites are highly bioactive molecules that affect various cellular functions including differentiation, cellular senescence, apoptosis, and proliferation when added exogenously, or elevated intracellularly by turnover of complex sphingolipids or synthesis from de novo pathway. We are investigating the relationship of sphingolipids cycle in apoptosis early events. A new column liquid chromatography- tandem mass spectrometry (LC/MS/MS) in combination with multiple reaction monitoring (MRM) method was developed for the rapid, simultaneous and quantitative determination of unambiguous detecting sphingolipids in cells. (omitted)

• Molecules and Cells
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• v.38 no.6
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• pp.482-495
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• 2015

Sphingolipids such as ceramide, sphingosine-1-phosphate and sphingomyelin have been emerging as bioactive lipids since ceramide was reported to play a role in human leukemia HL-60 cell differentiation and death. Recently, it is well-known that ceramide acts as an inducer of cell death, that sphingomyelin works as a regulator for microdomain function of the cell membrane, and that sphingosine-1-phosphate plays a role in cell survival/proliferation. The lipids are metabolized by the specific enzymes, and each metabolite could be again returned to the original form by the reverse action of the different enzyme or after a long journey of many metabolizing/synthesizing pathways. In addition, the metabolites may serve as reciprocal biomodulators like the rheostat between ceramide and sphingosine-1-phosphate. Therefore, the change of lipid amount in the cells, the subcellular localization and the downstream signal in a specific subcellular organelle should be clarified to understand the pathobiological significance of sphingolipids when extracellular stimulation induces a diverse of cell functions such as cell death, proliferation and migration. In this review, we focus on how sphingolipids and their metabolizing enzymes cooperatively exert their function in proliferation, migration, autophagy and death of hematopoetic cells, and discuss the way developing a novel therapeutic device through the regulation of sphingolipids for effectively inhibiting cell proliferation and inducing cell death in hematological malignancies such as leukemia, malignant lymphoma and multiple myeloma.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.271.1-271.1
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• 2002

Sphingolipids have been emerged as bioactive lipid modulators that mediate a variety of cell functions. However. the effects of sphingolipids on the cell growth and survival of melanocytes are not yet known. In the present study, we investigated the actions of sphingolipids in Mel-Ab melanocytes. We observed the cytoprotective effect of sphingosine-1-phosphate (SPP) on UVB-induced cell death. (omitted)

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.162.1-162.1
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• 2003

The purpose of this study was to determine the possibility of sphingolipid as a diagnostic marker for Myocardiac Infarction(MI), atherosclerosis-related cardiovascular disease. Sphingolipids are known to playa role in the occurrence of atherosclerosis in human blood vessels. Platelet-poor plasma(PPP) and washed platelets were prepared from healthy volunteers and MI patients, and sphingolipids analyzed. (omitted)

• Proceedings of the SCSK Conference
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• 2003.09a
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• pp.498-498
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• 2003

Sphingolipids are important structural components of the stratum corneum lipids and serve the epidermal permeability barrier function. Recent investigations on biological activities of sphingolipids have revealed that they have a number of important biological functions in the cell such as cell proliferation and differentiation, anti-inflammation, mediation of signal transduction and many more.(omitted)

• Biomolecules & Therapeutics
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• v.29 no.4
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• pp.373-383
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• 2021

Atherosclerosis is the deposition of plaque in the main arteries. It is an inflammatory condition involving the accumulation of macrophages and various lipids (low-density lipoprotein [LDL] cholesterol, ceramide, S1P). Moreover, endothelial cells, macrophages, leukocytes, and smooth muscle cells are the major players in the atherogenic process. Sphingolipids are now emerging as important regulators in various pathophysiological processes, including the atherogenic process. Various sphingolipids exist, such as the ceramides, ceramide-1-phosphate, sphingosine, sphinganine, sphingosine-1-phosphate (S1P), sphingomyelin, and hundreds of glycosphingolipids. Among these, ceramides, glycosphingolipids, and S1P play important roles in the atherogenic processes. The atherosclerotic plaque consists of higher amounts of ceramide, glycosphingolipids, and sphingomyelin. The inhibition of the de novo ceramide biosynthesis reduces the development of atherosclerosis. S1P regulates atherogenesis via binding to the S1P receptor (S1PR). Among the five S1PRs (S1PR1-5), S1PR1 and S1PR3 mainly exert anti-atherosclerotic properties. This review mainly focuses on the effects of ceramide and S1P via the S1PR in the development of atherosclerosis. Moreover, it discusses the recent findings and potential therapeutic implications in atherosclerosis.

• BMB Reports
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• v.39 no.2
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• pp.113-131
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• 2006

Sphingolipids have emerged as molecules whose metabolism is regulated leading to generation of bioactive products including ceramide, sphingosine, and sphingosine-1-phosphate. The balance between cellular levels of these bioactive products is increasingly recognized to be critical to cell regulation; whereby, ceramide and sphingosine cause apoptosis and growth arrest phenotypes, and sphingosine-1-phosphate mediates proliferative and angiogenic responses. Sphingosine kinase is a key enzyme in modulating the levels of these lipids and is emerging as an important and regulated enzyme. This review is geared at mechanisms of regulation of sphingosine kinase and the coming to light of its role in disease.

• Biomolecules & Therapeutics
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• v.22 no.2
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• pp.83-92
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• 2014

Fatty acids (FAs) are highly diverse in terms of carbon (C) chain-length and number of double bonds. FAs with C>20 are called very long-chain fatty acids (VLCFAs). VLCFAs are found not only as constituents of cellular lipids such as sphingolipids and glycerophospholipids but also as precursors of lipid mediators. Our understanding on the function of VLCFAs is growing in parallel with the identification of enzymes involved in VLCFA synthesis or degradation. A variety of inherited diseases, such as ichthyosis, macular degeneration, myopathy, mental retardation, and demyelination, are caused by mutations in the genes encoding VLCFA metabolizing enzymes. In this review, we describe mammalian VLCFAs by highlighting their tissue distribution and metabolic pathways, and we discuss responsible genes and enzymes with reference to their roles in pathophysiology.