May 18, 2024

Schulze C, Smales C, Rubin LL, Staddon JM

Schulze C, Smales C, Rubin LL, Staddon JM. prostanoids, epoxyeicosatrienoic acids, sphingolipids, and lysophospholipids, contribute to vascular function and signaling within the endothelium. Methods for quantifying lipids will become briefly discussed, followed by an overview of the various lipid family members. The cross talk in signaling between classes of lipids will become discussed in the context of vascular disease. Finally, the potential medical implications of these lipid family members will become highlighted. double bonds of arachidonic acid allow it to react with three oxygenases to form different subtypes of eicosanoids, including prostaglandins, epoxyeicosatrienoic acids, and leukotrienes. Consequently, while methods that do not require lipid extraction may result in higher yield, these methods often lack specificity to distinguish between isoforms within the same lipid family. For these reasons, the method of choice for lipid measurement should be chosen on the basis of the specific question becoming addressed. Some of the earliest bioassays for lipid quantification relied on assessment of biological activity with the assumption that activity was directly correlated to concentration (147). These results were indicated as lipid-equivalent levels. Unfortunately, this strategy does not are the cause of volume of distribution, activity, and degree of metabolite formation, binding affinity, and membrane permeability, each of which needs to be considered for precise measurement. Relevant to the study of the microcirculation, more recent methods have been developed that rely on radiolabeling, fluorescence detection, and measurement of absorbance (colorimetric assays) to quantify lipids of interest. While these methods will not be extensively examined here, brief explanations, as well as improvements and pitfalls, for each of these methods will become briefly pointed out below and are summarized in Table 1. The reader interested in a more detailed explanation of advantages and weaknesses of these assays is referred to several superb citations (1, 61, 86, 99, 145). Table 1. Various methods to measure bioactive lipids 19: 6732018, 2018.] doi:10.1038/nrm.2017.107. [PMC free article] [PubMed] [CrossRef] [Google Scholar] 50. Harizi H, Corcuff JB, Gualde N. Arachidonic-acid-derived eicosanoids: functions in biology and immunopathology. Styles Mol Med 14: 461C469, 2008. doi:10.1016/j.molmed.2008.08.005. [PubMed] [CrossRef] [Google Scholar] 51. Haserck N, Erl W, Pandey D, Tigyi G, Ohlmann P, Ravanat C, Gachet C, Siess W. The plaque lipid lysophosphatidic acid stimulates platelet activation and platelet-monocyte aggregate formation in whole blood: involvement of P2Y1 and P2Y12 receptors. Blood 103: 2585C2592, 2004. doi:10.1182/blood-2003-04-1127. [PubMed] [CrossRef] [Google Scholar] 52. Havulinna AS, Sysi-Aho M, Hilvo M, Kauhanen D, Hurme R, Ekroos K, Salomaa V, Laaksonen R. Circulating ceramides forecast cardiovascular results in the population-based FINRISK 2002 cohort. Arterioscler Thromb Vasc Biol 36: 2424C2430, 2016. doi:10.1161/ATVBAHA.116.307497. [PubMed] [CrossRef] [Google Scholar] 53. Holland WL, Summers SA. Sphingolipids, insulin resistance, and metabolic disease: fresh insights from in vivo manipulation of sphingolipid rate of metabolism. Endocr Rev 29: 381C402, 2008. doi:10.1210/er.2007-0025. [PMC free article] [PubMed] [CrossRef] [Google Scholar] 54. Hosogaya S, Yatomi Y, Nakamura K, Ohkawa R, Okubo S, Yokota H, Ohta M, Yamazaki H, Koike T, Ozaki Y. Measurement of plasma lysophosphatidic acid concentration in healthy subjects: strong correlation with lysophospholipase D activity. Ann Clin Biochem 45: 364C368, 2008. doi:10.1258/acb.2008.007242. [PubMed] [CrossRef] [Google Scholar] 55. Huang H, Weng J, Wang MH. EETs/sEH in diabetes and obesity-induced cardiovascular diseases. Prostaglandins Additional Lipid Mediat 125: 80C89, 2016. doi:10.1016/j.prostaglandins.2016.05.004. [PubMed] [CrossRef] [Google Scholar] 56. Huang X, Withers BR, Dickson RC. Sphingolipids and lifespan regulation. Biochim Biophys Acta 1841: 657C664, 2014. doi:10.1016/j.bbalip.2013.08.006. [PMC free article] [PubMed] [CrossRef] [Google Scholar] 57. Imig JD, Dimitropoulou C, Reddy DS, White colored RE, Falck JR. Afferent arteriolar dilation to 11, 12-EET analogs entails PP2A activity and Ca2+-triggered K+ channels. 15: 137C150, 2008. doi:10.1080/10739680701456960. [PMC free article] [PubMed] [CrossRef] [Google Scholar] 58. Imig JD, Hammock BD. Soluble epoxide hydrolase like a restorative target for cardiovascular diseases. Nat Rev Drug Discov 8: 794C805, 2009. doi:10.1038/nrd2875. [PMC free article] [PubMed] [CrossRef] [Google Scholar] 59. Imig JD, Zhao X, Capdevila JH, Morisseau C, Hammock BD. Soluble epoxide hydrolase inhibition lowers arterial blood pressure in angiotensin II hypertension. Hypertension 39: 690C694, 2002. doi:10.1161/hy0202.103788. [PubMed] [CrossRef] [Google Scholar] 60. Imig JD, Zhao X, Zaharis CZ, Olearczyk JJ, Pollock DM, Newman JW, Kim IH, Watanabe T, Hammock BD. An orally active epoxide hydrolase inhibitor lowers blood pressure and provides renal safety in salt-sensitive hypertension. Hypertension 46: 975C981, 2005..Cardiovasc Diabetol 12: 27, 2013. lipids will become briefly discussed, followed by an overview of the various lipid family members. The cross talk in signaling between classes of lipids will become discussed in the context of vascular disease. Finally, the potential clinical AB-MECA implications of these lipid family members will become highlighted. double bonds of arachidonic acid allow it to react with three oxygenases to form TNFRSF9 different subtypes of eicosanoids, including prostaglandins, epoxyeicosatrienoic acids, and leukotrienes. Consequently, while methods that do not require lipid extraction may result in higher yield, these methods often lack specificity to distinguish between isoforms within the same lipid family. AB-MECA For these reasons, the method of choice for lipid measurement should be chosen on the basis of the specific question becoming addressed. Some of the earliest bioassays for lipid quantification relied on assessment of biological activity with the assumption that activity was directly correlated to concentration (147). These results were indicated as lipid-equivalent levels. Unfortunately, this strategy does not are the cause of volume of distribution, activity, and degree of metabolite formation, binding affinity, and membrane permeability, each of which must be considered for precise measurement. Relevant to the study of the microcirculation, more recent methods have been developed that rely on radiolabeling, fluorescence detection, and measurement of absorbance (colorimetric assays) to quantify lipids of interest. While these methods will not be extensively reviewed here, brief explanations, as well as improvements and pitfalls, for each of these methods will become briefly pointed out below and are summarized in Table 1. The reader interested in a more detailed explanation of advantages and weaknesses of these assays is referred to several superb citations (1, 61, 86, 99, 145). Table 1. Various methods to measure bioactive lipids 19: 6732018, 2018.] doi:10.1038/nrm.2017.107. [PMC free article] [PubMed] [CrossRef] [Google Scholar] 50. Harizi H, Corcuff JB, Gualde N. Arachidonic-acid-derived eicosanoids: functions in biology and immunopathology. Styles Mol Med 14: 461C469, 2008. doi:10.1016/j.molmed.2008.08.005. [PubMed] [CrossRef] [Google Scholar] 51. Haserck N, Erl W, Pandey D, Tigyi G, Ohlmann P, Ravanat C, Gachet C, Siess W. The plaque lipid lysophosphatidic acid stimulates platelet activation and platelet-monocyte aggregate formation in whole blood: involvement of P2Y1 and P2Y12 receptors. Blood 103: 2585C2592, 2004. doi:10.1182/blood-2003-04-1127. [PubMed] [CrossRef] [Google Scholar] 52. Havulinna AS, Sysi-Aho M, Hilvo M, Kauhanen D, Hurme R, Ekroos K, Salomaa V, Laaksonen R. Circulating ceramides forecast cardiovascular results in the population-based FINRISK 2002 cohort. Arterioscler Thromb Vasc Biol 36: 2424C2430, 2016. doi:10.1161/ATVBAHA.116.307497. [PubMed] [CrossRef] [Google Scholar] 53. Holland WL, Summers SA. Sphingolipids, insulin resistance, and metabolic disease: fresh insights from in vivo manipulation of sphingolipid rate of metabolism. Endocr Rev 29: 381C402, 2008. doi:10.1210/er.2007-0025. [PMC free article] [PubMed] [CrossRef] [Google Scholar] 54. Hosogaya S, Yatomi Y, Nakamura K, Ohkawa R, Okubo S, Yokota H, Ohta M, Yamazaki H, Koike T, Ozaki Y. Measurement of plasma lysophosphatidic acid concentration in healthy subjects: strong correlation with lysophospholipase D activity. Ann Clin Biochem 45: 364C368, 2008. doi:10.1258/acb.2008.007242. [PubMed] [CrossRef] [Google Scholar] 55. Huang H, Weng J, Wang MH. EETs/sEH in diabetes and obesity-induced cardiovascular diseases. Prostaglandins Additional Lipid Mediat 125: 80C89, 2016. doi:10.1016/j.prostaglandins.2016.05.004. [PubMed] [CrossRef] [Google Scholar] 56. Huang X, Withers BR, Dickson RC. Sphingolipids and life-span rules. Biochim Biophys Acta 1841: 657C664, 2014. doi:10.1016/j.bbalip.2013.08.006. [PMC free article] [PubMed] [CrossRef] [Google Scholar] 57. Imig JD, Dimitropoulou C, Reddy DS, White colored RE, Falck JR. Afferent arteriolar dilation to 11, 12-EET analogs entails PP2A activity and Ca2+-triggered K+ channels. 15: 137C150, 2008. doi:10.1080/10739680701456960. [PMC free article] [PubMed] [CrossRef] [Google Scholar] 58. Imig JD, Hammock.Prostacyclin and endothelium-dependent hyperpolarization. also important for avoiding vascular dysfunction following malignancy treatment, a rapidly growing problem in medical oncology. The purpose of this review is usually to discuss how biologically active lipids, specifically prostanoids, epoxyeicosatrienoic acids, sphingolipids, and lysophospholipids, contribute to vascular function and signaling AB-MECA within the endothelium. Methods for quantifying lipids will be briefly discussed, followed by an overview of the various lipid families. The cross talk in signaling between classes of lipids will be discussed in the context of vascular disease. Finally, the potential clinical implications of these lipid families will be highlighted. double bonds of arachidonic acid allow it to react with three oxygenases to form different subtypes of eicosanoids, including prostaglandins, epoxyeicosatrienoic acids, and leukotrienes. Therefore, while methods that do not require lipid extraction may result in higher yield, these methods often lack specificity to distinguish between isoforms within the same lipid family. For these reasons, the method of choice for lipid measurement should be chosen on the basis of the specific question being addressed. Some of the earliest bioassays for lipid quantification relied on comparison of biological activity with the assumption that activity was directly correlated to concentration (147). These results were expressed as lipid-equivalent levels. Unfortunately, this methodology does not take into account volume of distribution, activity, and extent of metabolite formation, binding affinity, and membrane permeability, each of which needs to be considered for precise measurement. Relevant to the study of the microcirculation, more recent methods have been developed that rely on radiolabeling, fluorescence detection, and measurement of absorbance (colorimetric assays) to quantify lipids of interest. While these methods will not be extensively reviewed here, brief explanations, as well as advances and pitfalls, for each of these methods will be briefly mentioned below and are summarized in Table 1. The reader interested in a more detailed explanation of strengths and weaknesses of these assays is referred to several excellent citations (1, 61, 86, 99, 145). Table 1. Various methods to measure bioactive lipids 19: 6732018, 2018.] doi:10.1038/nrm.2017.107. [PMC free article] [PubMed] [CrossRef] [Google Scholar] 50. Harizi H, Corcuff JB, Gualde N. Arachidonic-acid-derived eicosanoids: roles in biology and immunopathology. Trends Mol Med 14: 461C469, 2008. doi:10.1016/j.molmed.2008.08.005. [PubMed] [CrossRef] [Google Scholar] 51. Haserck N, Erl W, Pandey D, Tigyi G, Ohlmann P, Ravanat C, Gachet C, Siess W. The plaque lipid lysophosphatidic acid stimulates platelet activation and platelet-monocyte aggregate formation in whole blood: involvement of P2Y1 and P2Y12 receptors. Blood 103: 2585C2592, 2004. doi:10.1182/blood-2003-04-1127. [PubMed] [CrossRef] [Google Scholar] 52. Havulinna AS, Sysi-Aho M, Hilvo M, Kauhanen D, Hurme R, Ekroos K, Salomaa V, Laaksonen R. Circulating ceramides predict cardiovascular outcomes in the population-based FINRISK 2002 cohort. Arterioscler Thromb Vasc Biol 36: 2424C2430, 2016. doi:10.1161/ATVBAHA.116.307497. [PubMed] [CrossRef] [Google Scholar] 53. Holland WL, Summers SA. Sphingolipids, insulin resistance, and metabolic disease: new insights from in vivo manipulation of sphingolipid metabolism. Endocr Rev 29: 381C402, 2008. doi:10.1210/er.2007-0025. [PMC free article] [PubMed] [CrossRef] [Google Scholar] 54. Hosogaya S, Yatomi Y, Nakamura K, Ohkawa R, Okubo S, Yokota H, Ohta M, Yamazaki H, Koike T, Ozaki Y. Measurement of plasma lysophosphatidic acid concentration in healthy subjects: strong correlation with lysophospholipase D activity. Ann Clin Biochem 45: 364C368, 2008. doi:10.1258/acb.2008.007242. [PubMed] [CrossRef] [Google Scholar] 55. Huang H, Weng J, Wang MH. EETs/sEH in diabetes and obesity-induced cardiovascular diseases. Prostaglandins Other Lipid Mediat 125: 80C89, 2016. doi:10.1016/j.prostaglandins.2016.05.004. [PubMed] [CrossRef] [Google Scholar] 56. Huang X, Withers BR, Dickson RC. Sphingolipids and lifespan regulation. Biochim Biophys Acta 1841: 657C664, 2014. doi:10.1016/j.bbalip.2013.08.006. [PMC free article] [PubMed] [CrossRef] [Google Scholar] 57. Imig JD, Dimitropoulou C, Reddy DS,.