Induction of insulin secretion by apolipoprotein M, a carrier for sphingosine 1-phosphate

Kurano, Makoto; Hara, Mariko; Tsuneyama, Koichi; Sakoda, Hideyuki; Shimizu, Tomo; Tsukamoto, Kazuhisa; Ikeda, Hitoshi; Yatomi, Yutaka

doi:10.1016/j.bbalip.2014.05.002

Cited by 57 publications

(64 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Although data are limited at present, several papers have proposed that S1P bound to ApoM also possesses physiologic properties different from those of S1P bound to albumin for several physiologic properties other than cell proliferation and fibrosis; S1P bound to ApoM on HDL has a greater effect in maintaining the endothelial barrier (61) and on the secretion of insulin from pancreatic β‐cells (33), whereas S1P carried on ApoM has a suppressive effect on the inflammation of endothelial cells (16) and the induction of PAI‐1 (62), suggesting that the protective properties of S1P against human disorders may be augmented when bound to ApoM, whereas the harmful aspects of S1P in general may be attenuated. Whether S1P possesses beneficial or harmful properties in terms of human diseases has been controversial.…”

Section: Discussionmentioning

confidence: 99%

“…Since 2011, when ApoM was first ABBREVIATIONS: ApoM, apolipoprotein M; BW, body weight; Col, collagen; Ctgf, connective tissue growth factor; FBS, fetal bovine serum; Fn, fibronectin; GFP, green fluorescent protein; HIGA, hyper-IgA; KO, knockout; PAS, periodic acid-Schiff; PTX, pertussis toxin; rApoM, recombinant ApoM; S1P, sphingosine 1-phosphate; siApoM, small interfering RNA against murine ApoM; siCtl, control siRNA; WT, wild type established as a carrier of S1P (25), we and others have demonstrated that ApoM is not actually a carrier of S1P, but rather is a modulator of S1P metabolism, and S1P bound to albumin is unstable in plasma, whereas S1P bound to ApoM is stable (30)(31)(32). We were able to modulate the plasma S1P levels continuously using the adenoviral gene transfer of ApoM or the knockdown of ApoM in an in vivo siRNA system (33,34). The epidemiologic association between HDL and the progression of chronic kidney diseases also prompted us to investigate the association between S1P and IgA nephropathy (35,36).…”

mentioning

confidence: 89%

“…Since 2011, when ApoM was first established as a carrier of S1P (25), we and others have demonstrated that ApoM is not actually a carrier of S1P, but rather is a modulator of S1P metabolism, and S1P bound to albumin is unstable in plasma, whereas S1P bound to ApoM is stable (30–32). We were able to modulate the plasma S1P levels continuously using the adenoviral gene transfer of ApoM or the knockdown of ApoM in an in vivo siRNA system (33, 34). The epidemiologic association between HDL and the progression of chronic kidney diseases also prompted us to investigate the association between S1P and IgA nephropathy (35, 36).…”

mentioning

confidence: 99%

See 2 more Smart Citations

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

et al. 2019

Self Cite

View full text Add to dashboard Cite

Because the association between sphingosine 1‐phosphate (S1P)/apolipoprotein M (ApoM) and chronic kidney diseases has not been established, we investigated the involvement of S1P/ApoM in the phenotypes of IgA nephropathy in hyper‐IgA (HIGA) mice. The overexpression of ApoM in adenoviral gene transfer ameliorated the phenotypes of IgA nephropathy in HIGA mice, whereas the knockdown of ApoM with siRNA caused deterioration. When ApoM‐overexpressing HIGA mice were treated with VPC23019, an antagonist against S1P receptor 1 (S1P1) and 3 (S1P3), we observed that the protective effects of ApoM were reversed, whereas JTE013, an antagonist against S1P2, did not inhibit the effects. We also found that S1P bound to albumin accelerated the proliferation of MES13 cells and the fibrotic changes of HK2 cells, which were inhibited by JTE013, whereas S1P bound to ApoM suppressed these changes, which were inhibited by VPC23019. These results suggest that S1P bound to ApoM possesses properties protective against the phenotypes of IgA nephropathy through S1P1 and S1P3, whereas S1P bound to albumin exerts deteriorating effects through S1P2. ApoM may be useful as a therapeutic target to treat or retard the progression of IgA nephropathy.—Kurano, M., Tsuneyama, K., Morimoto, Y., Nishikawa, M., Yatomi, Y. Apolipoprotein M suppresses the phenotypes of IgA nephropathy in hyper‐IgA mice. FASEB J. 33, 5181–5195 (2019). http://www.fasebj.org

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 89%

mentioning

confidence: 99%

See 1 more Smart Citation

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

et al. 2019

Self Cite

View full text Add to dashboard Cite

show abstract

“…In the plasma, S1P is carried by apolipoprotein M in a complex with high-density lipoprotein (HDL) (Christoffersen et al 2011). Apolipoprotein M not only functions as a vehicle to carry and deliver its S1P to different tissues but to also stimulate S1P synthesis in the liver (Liu et al 2014) and to induce insulin secretion (Kurano et al 2014).…”

Section: Sphingolipid Metabolismmentioning

confidence: 99%

Resveratrol and its oligomers: modulation of sphingolipid metabolism and signaling in disease

et al. 2014

View full text Add to dashboard Cite

Resveratrol, a natural compound endowed with multiple health-promoting effects, has received much attention given its potential for the treatment of cardiovascular, inflammatory, neurodegenerative, metabolic and age-related diseases. However, the translational potential of resveratrol has been limited by its specificity, poor bioavailability and uncertain toxicity. In recent years, there has been an accumulation of evidence demonstrating that resveratrol modulates sphingolipid metabolism. Moreover, resveratrol forms higher order oligomers that exhibit better selectivity and potency in modulating sphingolipid metabolism. This review evaluates the evidence supporting the modulation of sphingolipid metabolism and signaling as a mechanism of action underlying the therapeutic efficacy of resveratrol and oligomers in diseases, such as cancer.

show abstract

“…More recent studies have extended the potential impact of HDL-S1P to other cells, including pancreatic beta cells, where it was shown to improve insulin secretion, notably under conditions of endoreticulum stress. 41 …”

Section: D F Ementioning

confidence: 99%

Diabetes Mellitus Is Associated With Reduced High-Density Lipoprotein Sphingosine-1-Phosphate Content and Impaired High-Density Lipoprotein Cardiac Cell Protection

Brinck

Thomas

Lauer

et al. 2016

ATVB

View full text Add to dashboard Cite

Objective— The dyslipidemia of type 2 diabetes mellitus has multiple etiologies and impairs lipoprotein functionality, thereby increasing risk for cardiovascular disease. High-density lipoproteins (HDLs) have several beneficial effects, notably protecting the heart from myocardial ischemia. We hypothesized that glycation of HDL could compromise this cardioprotective effect. Approach and Results— We used in vitro (cardiomyocytes) and ex vivo (whole heart) models subjected to oxidative stress together with HDL isolated from diabetic patients and nondiabetic HDL glycated in vitro (methylglyoxal). Diabetic and in vitro glycated HDL were less effective ( P <0.05) than control HDL in protecting from oxidative stress. Protection was significantly, inversely correlated with the degree of in vitro glycation ( P <0.001) and the levels of hemoglobin A1c in diabetic patients ( P <0.007). The ability to activate protective, intracellular survival pathways involving Akt, Stat3, and Erk1/2 was significantly reduced ( P <0.05) using glycated HDL. Glycation reduced the sphingosine-1-phosphate (S1P) content of HDL, whereas the S1P concentrations of diabetic HDL were inversely correlated with hemoglobin A1c ( P <0.005). The S1P contents of in vitro glycated and diabetic HDL were significantly, positively correlated (both <0.01) with cardiomyocyte survival during oxidative stress. Adding S1P to diabetic HDL increased its S1P content and restored its cardioprotective function. Conclusions— Our data demonstrate that glycation can reduce the S1P content of HDL, leading to increased cardiomyocyte cell death because of less effective activation of intracellular survival pathways. It has important implications for the functionality of HDL in diabetes mellitus because HDL-S1P has several beneficial effects on the vasculature.

show abstract

Induction of insulin secretion by apolipoprotein M, a carrier for sphingosine 1-phosphate

Abstract: ApoM augmented insulin secretion by maintaining the S1P concentration under both in vivo and in vitro conditions.

Cited by 57 publications

References 39 publications

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

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

Resveratrol and its oligomers: modulation of sphingolipid metabolism and signaling in disease

Diabetes Mellitus Is Associated With Reduced High-Density Lipoprotein Sphingosine-1-Phosphate Content and Impaired High-Density Lipoprotein Cardiac Cell Protection

Contact Info

Product

Resources

About