Apolipoprotein M suppresses the phenotypes of IgA nephropathy in hyper‐IgA mice

Kurano, Makoto; Tsuneyama, Koichi; Morimoto, Yuki; Nishikawa, Masako; Yatomi, Yutaka

doi:10.1096/fj.201801748r

Cited by 25 publications

(23 citation statements)

References 65 publications

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“…However, in these studies, the S1P levels were modulated by delivering S1P using albumin as the vehicle or by modulating the level of an enzyme involved in the production of S1P. Recently, several articles have demonstrated that S1P bound to apoM/HDL might possess different properties from S1P bound to albumin; S1P bound to apoM/HDL might be a biased agonist for S1P1 and/or S1P3 (10,15,(35)(36)(37). Considering that several previous studies have reported that insulin resistance is induced by the activation of S1P2 (32), the results of the current study were not contrary to these reports.…”

Section: Discussionmentioning

confidence: 99%

Protection Against Insulin Resistance by Apolipoprotein M/Sphingosine-1-Phosphate

et al. 2020

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Subjects with low serum HDL cholesterol levels are reported to be susceptible to diabetes, with insulin resistance believed to be the underlying pathological mechanism. Apolipoprotein M (apoM) is a carrier of sphingosine-1-phosphate (S1P), a multifunctional lipid mediator, on HDL, and the pleiotropic effects of HDL are believed to be mediated by S1P. In the current study, we attempted to investigate the potential association between apoM/S1P and insulin resistance. We observed that the serum levels of apoM were lower in patients with type 2 diabetes and that they were negatively correlated with BMI and the insulin resistance index. While deletion of apoM in mice was associated with worsening of insulin resistance, overexpression of apoM was associated with improvement of insulin resistance. Presumably, apoM/S1P exerts its protective effect against insulin resistance by activating insulin signaling pathways, such as the AKT and AMPK pathways, and also by improving the mitochondrial functions through upregulation of SIRT1 protein levels. These actions of apoM/S1P appear to be mediated via activation of S1P1 and/or S1P3. These results suggest that apoM/S1P exerts protective roles against the development of insulin resistance.

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Section: Discussionmentioning

confidence: 99%

Protection Against Insulin Resistance by Apolipoprotein M/Sphingosine-1-Phosphate

et al. 2020

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“…FTY720, an immunosuppressive S1PRs ligand that functions as S1PRs antagonist, prevents inflammatory alterations in ureteral obstruction and angiotensin II treatment models 83,84 . However, the S1P effects are diverse depending on receptor subtypes and pathological conditions 85,86 . For instance, SphK1/S1P/S1PR1 axis in endothelial cells and proximal tubular cells plays important roles in protecting against renal ischemia-reperfusion injury 37,87,88 The sFlt is believed to inhibit vasodilation and induce maternal hypertension by antagonizing vascular endothelial cell growth factor (VEGF) action to produce nitric oxide 95 .…”

Section: Inhibition Of Glucosylceramide Formation Suppresses Pathologmentioning

confidence: 99%

Sphingolipids and Kidney Disease: Possible Role of Preeclampsia and Intrauterine Growth Restriction (IUGR)

et al. 2021

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Sphingolipids are now considered not only as constitutional components of the cellular membrane but also as essential bioactive factors regulating development and physiological functions. Ceramide is a vital intermediate of sphingolipid metabolism, synthesized by de novo and salvage pathways, producing multiple types of sphingolipids and their metabolites. Although mutations in gene encoding enzymes regulating sphingolipid synthesis and metabolism cause distinct diseases, an abnormal sphingolipid metabolism contributes to various pathological conditions, including kidney disease. Excessive accumulation of glycosphingolipids and promotion of the ceramide salvage and sphingosine-1-phosphate (S1P) pathways are found in the damaged kidney. Acceleration of the sphingosine kinase/S1P/S1P receptor (SphK/S1P/S1PR) axis plays a central role in deteriorating kidney functions. The SphK/S1P/S1PR signaling impairment is also found during pregnancy complications such as preeclampsia and intrauterine growth restriction (IUGR). This mini-review discusses the current state of knowledge regarding the role of sphingolipid metabolism on kidney diseases and the possible involvement of preeclampsia and IUGR conditions.

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“…In 2011, Christoffersen et al reported that apolipoprotein M (ApoM) is the main carrier of S1P on HDL 12) . We and others have demonstrated that ApoM is also an important modulator of S1P metabolism and functions [13][14][15][16][17][18][19][20][21][22] .…”

Section: Glycation Of Hdl and Anti-glycation Of Hdlmentioning

confidence: 99%

Glycation of HDL Polymerizes Apolipoprotein M and Attenuates Its Capacity to Bind to Sphingosine 1-Phosphate

Tamaki

Kurano

Nanya

et al. 2021

JAT

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The official journal of the Japan Atherosclerosis Society and the Asian Pacific Society of Atherosclerosis and Vascular Diseases Original Article Aim: Recently, it has been established that most of the pleiotropic effects of high-density lipoprotein (HDL) are attributed to sphingosine 1-phosphate (S1P), which rides on HDL via apolipoprotein M (ApoM). In subjects with diabetes mellitus, both the pleiotropic effects of HDL and its role in reverse cholesterol transport are reported to be impaired. To elucidate the mechanisms underlying the impaired pleiotropic effects of HDL in subjects with diabetes, from the aspects of S1P and ApoM. Methods: The incubation of HDL in a high-glucose condition resulted in the dimerization of ApoM. Moreover, the treatment of HDL with methylglyoxal resulted in the modulation of the ApoM structure, as suggested by the results of western blot analysis, isoelectric focusing electrophoresis, and two-dimensional gel electrophoresis, which was reversed by treatment with anti-glycation reagents. Results: The glycation of HDL resulted in impaired binding of the glycated HDL to S1P, and the S1P on glycated HDL degraded faster. In the case of human subjects, on the other hand, although both the serum ApoM levels and the ApoM content in HDL were lower in subjects with diabetes, we did not observe the polymerization of ApoM. Conclusions: Modulation of the quantity and quality of ApoM might explain, at least in part, the impaired functions of HDL in subjects with diabetes mellitus. ApoM might be a useful target for laboratory testing and/or the treatment of diabetes mellitus. has been reported to exert many pleiotropic effects, such as antiapoptotic, anti-inflammatory, and vasoprotective effects 1). The relatively low levels of HDL in subjects with diabetes may explain, at least in part, the high prevalence of atherosclerotic diseases in these subjects 2). In addition to the quantitative abnormality

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Apolipoprotein M suppresses the phenotypes of IgA nephropathy in hyper‐IgA mice

Cited by 25 publications

References 65 publications

Protection Against Insulin Resistance by Apolipoprotein M/Sphingosine-1-Phosphate

Protection Against Insulin Resistance by Apolipoprotein M/Sphingosine-1-Phosphate

Sphingolipids and Kidney Disease: Possible Role of Preeclampsia and Intrauterine Growth Restriction (IUGR)

Glycation of HDL Polymerizes Apolipoprotein M and Attenuates Its Capacity to Bind to Sphingosine 1-Phosphate

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