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Article: The role of sphingosine-1-phosphate in endothelial barrier function.

Wilkerson, Brent A / Argraves, Kelley M

2014 Volume 1841, Issue 10, Page(s) 1403–1412

Abstract: Loss of endothelial barrier function is implicated in the etiology of metastasis, atherosclerosis, sepsis and many other diseases. Studies suggest that sphingosine-1-phosphate (S1P), particularly HDL-bound S1P (HDL-S1P) is essential for endothelial ... ...

Abstract	Loss of endothelial barrier function is implicated in the etiology of metastasis, atherosclerosis, sepsis and many other diseases. Studies suggest that sphingosine-1-phosphate (S1P), particularly HDL-bound S1P (HDL-S1P) is essential for endothelial barrier homeostasis and that HDL-S1P may be protective against the loss of endothelial barrier function in disease. This review summarizes evidence providing mechanistic insights into how S1P maintains endothelial barrier function, highlighting the recent findings that implicate the major S1P carrier, HDL, in the maintenance of the persistent S1P-signaling needed to maintain endothelial barrier function. We review the mechanisms proposed for HDL maintenance of persistent S1P-signaling, the evidence supporting these mechanisms and the remaining fundamental questions.
Language	English
Publishing date	2014-07-05
Publishing country	Netherlands
Document type	Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbalip.2014.06.012
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Article: HDL serves as a S1P signaling platform mediating a multitude of cardiovascular effects.

Argraves, Kelley M / Argraves, W Scott

Journal of lipid research

2007 Volume 48, Issue 11, Page(s) 2325–2333

Abstract: The lysosphingolipid sphingosine 1-phosphate (S1P) is a component of HDL. Findings from a growing number of studies indicate that S1P is a mediator of many of the cardiovascular effects of HDL, including the ability to promote vasodilation, ... ...

Abstract	The lysosphingolipid sphingosine 1-phosphate (S1P) is a component of HDL. Findings from a growing number of studies indicate that S1P is a mediator of many of the cardiovascular effects of HDL, including the ability to promote vasodilation, vasoconstriction, and angiogenesis, protect against ischemia/reperfusion injury, and inhibit/reverse atherosclerosis. These latter cardioprotective effects are being shown to involve the S1P-mediated suppression of inflammatory processes, including reduction of the endothelial expression of monocyte and lymphocyte adhesion molecules, decreased recruitment of polymorphonuclear cells to sites of infarction, and blocking of cardiomyocyte apoptosis after myocardial infarction. This review article summarizes the evidence that S1P as a component of HDL serves to regulate vascular cell and lymphocyte behaviors associated with cardiovascular (patho)physiology.
MeSH term(s)	ATP-Binding Cassette Transporters/physiology ; Animals ; Atherosclerosis/etiology ; Cardiovascular System/drug effects ; Cell Movement/drug effects ; Cystic Fibrosis Transmembrane Conductance Regulator/physiology ; Endothelial Cells/drug effects ; Endothelial Cells/physiology ; Humans ; Immunologic Factors/physiology ; Lipoproteins, HDL/physiology ; Lysophospholipids/physiology ; Muscle, Smooth, Vascular/physiology ; Phosphotransferases (Alcohol Group Acceptor)/blood ; Reperfusion Injury/prevention & control ; Signal Transduction/physiology ; Sphingosine/analogs & derivatives ; Sphingosine/physiology ; Vasoconstriction/physiology ; Vasodilation/physiology
Chemical Substances	ATP-Binding Cassette Transporters ; Immunologic Factors ; Lipoproteins, HDL ; Lysophospholipids ; Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6) ; sphingosine 1-phosphate (26993-30-6) ; Phosphotransferases (Alcohol Group Acceptor) (EC 2.7.1.-) ; sphingosine kinase (EC 2.7.1.-) ; Sphingosine (NGZ37HRE42)
Language	English
Publishing date	2007-08-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
DOI	10.1194/jlr.R700011-JLR200
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Article ; Online: Sphingosine-1-phosphate signaling in vasculogenesis and angiogenesis.

Argraves, Kelley M / Wilkerson, Brent A / Argraves, W Scott

World journal of biological chemistry

2008 Volume 1, Issue 10, Page(s) 291–297

Abstract: Blood vessels either form de novo through the process of vasculogenesis or through angiogenesis that involves the sprouting and proliferation of endothelial cells in pre-existing blood vessels. A complex interactive network of signaling cascades ... ...

Abstract	Blood vessels either form de novo through the process of vasculogenesis or through angiogenesis that involves the sprouting and proliferation of endothelial cells in pre-existing blood vessels. A complex interactive network of signaling cascades downstream from at least three of the nine known G-protein-coupled sphingosine-1-phosphate (S1P) receptors act as a prime effector of neovascularization that occurs in embryonic development and in association with various pathologies. This review focuses on the current knowledge of the roles of S1P signaling in vasculogenesis and angiogenesis, with particular emphasis on vascular cell adhesion and motility responses.
Language	English
Publishing date	2008-10-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	2564793-3
ISSN	1949-8454 ; 1949-8454
ISSN (online)	1949-8454
ISSN	1949-8454
DOI	10.4331/wjbc.v1.i10.291
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Article ; Online: Fibulin-1 suppresses endothelial to mesenchymal transition in the proximal outflow tract.

Harikrishnan, Keerthi / Cooley, Marion A / Sugi, Yukiko / Barth, Jeremy L / Rasmussen, Lars M / Kern, Christine B / Argraves, Kelley M / Argraves, W Scott

Mechanisms of development

2015 Volume 136, Page(s) 123–132

Abstract: Endothelial to mesenchymal transition (EMT) that occurs during cardiac outflow tract (OFT) development is critical for formation of the semilunar valves. Fibulin-1 (Fbln1) is an extracellular matrix protein that is present at several sites of EMT, ... ...

Abstract	Endothelial to mesenchymal transition (EMT) that occurs during cardiac outflow tract (OFT) development is critical for formation of the semilunar valves. Fibulin-1 (Fbln1) is an extracellular matrix protein that is present at several sites of EMT, including the OFT (i.e., E9.5-10.5). The aim of this study was to determine the role of Fbln1 in EMT during the earliest events of OFT development. Examination of proximal OFT cushions in Fbln1 null embryos detected hypercellularity at both E9.5 (93% increase; p = 0.002) and E10.5 (43% increase; p = 0.01) as compared to wild type, suggesting that Fbln1 normally suppresses OFT endocardial cushion EMT. This was supported by studies of proximal OFT cushion explants, which showed that explants from Fbln1 null embryos displayed a 58% increase in cells migrating from the explants as compared to wild type (p = 0.005). We next evaluated the effects of Fbln1 deficiency on the expression of factors that regulate proximal OFT EMT. At E9.5, Fbln1 null proximal OFT endocardium and EMT-derived mesenchyme showed increased TGFβ2 (58% increase; p = 0.01) and increased Snail1-positive nuclei (27% increase; p = 0.0003). Histological examination of OFT cushions in Fbln1 null embryos (E9.5) also detected cells present in the cushion that were determined to be erythrocytes based on round morphology, autofluorescence, and positive staining for hemoglobin. Erythrocytes were also detected in Fbln1 null OFT cushions at E10.5. Together, the findings indicate that Fbln1 normally suppresses proximal OFT EMT preventing proximal cushion hypercellularity and blood cell accumulation.
MeSH term(s)	Animals ; Apoptosis ; Calcium-Binding Proteins/genetics ; Calcium-Binding Proteins/metabolism ; Cell Proliferation ; Endocardial Cushions/cytology ; Endocardial Cushions/metabolism ; Endocardium/cytology ; Endocardium/metabolism ; Extracellular Matrix Proteins/genetics ; Extracellular Matrix Proteins/metabolism ; Mice ; Mice, Knockout ; Myocardium/cytology ; Myocardium/metabolism
Chemical Substances	Calcium-Binding Proteins ; Extracellular Matrix Proteins ; fibulin
Language	English
Publishing date	2015-05
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1055986-3
ISSN	1872-6356 ; 0925-4773
ISSN (online)	1872-6356
ISSN	0925-4773
DOI	10.1016/j.mod.2014.12.005
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Article ; Online: Sphingosine 1-phosphate (S1P) carrier-dependent regulation of endothelial barrier: high density lipoprotein (HDL)-S1P prolongs endothelial barrier enhancement as compared with albumin-S1P via effects on levels, trafficking, and signaling of S1P1.

Wilkerson, Brent A / Grass, G Daniel / Wing, Shane B / Argraves, W Scott / Argraves, Kelley M

The Journal of biological chemistry

2012 Volume 287, Issue 53, Page(s) 44645–44653

Abstract: Sphingosine 1-phosphate (S1P) is a blood-borne lysosphingolipid that acts to promote endothelial cell (EC) barrier function. In plasma, S1P is associated with both high density lipoproteins (HDL) and albumin, but it is not known whether the carriers ... ...

Abstract	Sphingosine 1-phosphate (S1P) is a blood-borne lysosphingolipid that acts to promote endothelial cell (EC) barrier function. In plasma, S1P is associated with both high density lipoproteins (HDL) and albumin, but it is not known whether the carriers impart different effects on S1P signaling. Here we establish that HDL-S1P sustains EC barrier longer than albumin-S1P. We showed that the sustained barrier effects of HDL-S1P are dependent on signaling by the S1P receptor, S1P1, and involve persistent activation of Akt and endothelial NOS (eNOS), as well as activity of the downstream NO target, soluble guanylate cyclase (sGC). Total S1P1 protein levels were found to be higher in response to HDL-S1P treatment as compared with albumin-S1P, and this effect was not associated with increased S1P1 mRNA or dependent on de novo protein synthesis. Several pieces of evidence indicate that long term EC barrier enhancement activity of HDL-S1P is due to specific effects on S1P1 trafficking. First, the rate of S1P1 degradation, which is proteasome-mediated, was slower in HDL-S1P-treated cells as compared with cells treated with albumin-S1P. Second, the long term barrier-promoting effects of HDL-S1P were abrogated by treatment with the recycling blocker, monensin. Finally, cell surface levels of S1P1 and levels of S1P1 in caveolin-enriched microdomains were higher after treatment with HDL-S1P as compared with albumin-S1P. Together, the findings reveal S1P carrier-specific effects on S1P1 and point to HDL as the physiological mediator of sustained S1P1-PI3K-Akt-eNOS-sGC-dependent EC barrier function.
MeSH term(s)	Endothelium, Vascular/cytology ; Endothelium, Vascular/metabolism ; Human Umbilical Vein Endothelial Cells/metabolism ; Humans ; Lipoproteins, HDL/metabolism ; Lysophospholipids/metabolism ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Protein Transport ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Receptors, Lysosphingolipid/genetics ; Receptors, Lysosphingolipid/metabolism ; Serum Albumin/metabolism ; Signal Transduction ; Sphingosine/analogs & derivatives ; Sphingosine/metabolism
Chemical Substances	Lipoproteins, HDL ; Lysophospholipids ; Receptors, Lysosphingolipid ; Serum Albumin ; high density lipoprotein-1 ; sphingosine 1-phosphate (26993-30-6) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Sphingosine (NGZ37HRE42)
Language	English
Publishing date	2012-11-07
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M112.423426
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Article: The role of sphingosine-1-phosphate in endothelial barrier function

Wilkerson, Brent A / Kelley M. Argraves

BBA - Molecular and Cell Biology of Lipids. 2014 Oct., v. 1841

2014

Abstract	Loss of endothelial barrier function is implicated in the etiology of metastasis, atherosclerosis, sepsis and many other diseases. Studies suggest that sphingosine-1-phosphate (S1P), particularly HDL-bound S1P (HDLâS1P) is essential for endothelial barrier homeostasis and that HDLâS1P may be protective against the loss of endothelial barrier function in disease. This review summarizes evidence providing mechanistic insights into how S1P maintains endothelial barrier function, highlighting the recent findings that implicate the major S1P carrier, HDL, in the maintenance of the persistent S1P-signaling needed to maintain endothelial barrier function. We review the mechanisms proposed for HDL maintenance of persistent S1P-signaling, the evidence supporting these mechanisms and the remaining fundamental questions.
Keywords	atherosclerosis ; etiology ; high density lipoprotein ; homeostasis ; metastasis ; sepsis (infection)
Language	English
Dates of publication	2014-10
Size	p. 1403-1412.
Publishing place	Elsevier B.V.
Document type	Article
ISSN	1388-1981
DOI	10.1016/j.bbalip.2014.06.012
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: FTY720 inhibited proinflammatory cytokine release and osteoclastogenesis induced by Aggregatibacter actinomycetemcomitans.

Yu, Hong / Herbert, Bethany A / Valerio, Michael / Yarborough, Leigh / Hsu, Li-Chien / Argraves, Kelley M

Lipids in health and disease

2015 Volume 14, Page(s) 66

Abstract: ... M-CSF) and receptor activator of nuclear factor kappa-B ligand (RANKL) for three days ... with A. actinomycetemcomitans for 4 to 24 h. Control cells were treated with M-CSF alone with or without bacterial stimulation ...

Abstract	Background: Periodontitis is a bacteria-driven inflammatory bone loss disease. Previous studies showed that the oral pathogen Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) stimulated the generation of sphingosine 1 phosphate (S1P). In addition, S1P signaling regulated the migration of osteoclast precursors and affected osteoclastogenesis. Furthermore, treatment with FTY720 (also called fingolimod, a modulator of multiple S1P receptors) alleviated osteoporosis and suppressed arthritis in animals. This study determined the effect of FTY720 on proinflammatory cytokine production and osteoclastogenesis in murine bone marrow cells with or without A. actinomycetemcomitans stimulation. Methods: Murine bone marrow-derived monocytes and macrophages (BMMs) were treated with vehicle ethanol or FTY720, and were either unstimulated or stimulated for 0.5 to 6 h with A. actinomycetemcomitans. The protein levels of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α in the media of BMMs were quantified by enzyme-linked immunosorbent assay (ELISA). Protein expressions, including phosphorylated phosphoinositide 3-kinase (p-PI3K), p-Akt, p-extracellular signal-regulated kinase (p-ERK), PI3K, Akt, and ERK were evaluated by Western blot. In addition, murine bone marrow-derived pre-osteoclasts were treated with macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor kappa-B ligand (RANKL) for three days. Then the cells were treated with either vehicle or FTY720 and were either unstimulated or stimulated with A. actinomycetemcomitans for 4 to 24 h. Control cells were treated with M-CSF alone with or without bacterial stimulation. Osteoclasts were stained by tartrate-resistant acid phosphatase (TRAP) staining. The mRNA levels of osteoclastogenic factors, including nuclear factor of activated T-cells cytoplasmic calcineurin-dependent 1 (Nfatc1), cathepsin K (Ctsk), acid phosphatase 5 (Acp5), osteoclast-associated receptor (Oscar), and RANKL were quantified by quantitative real-time polymerase chain reaction (PCR). Results: FTY720 dose-dependently inhibited IL-1β, IL-6, and TNF-α protein levels induced by A. actinomycetemcomitans in BMMs compared with controls. Additionally, FTY720 attenuated p-PI3K, p-Akt, and p-ERK expressions induced by A. actinomycetemcomitans. Furthermore, FTY720 suppressed osteoclastogenesis in bone marrow-derived pre-osteoclasts with or without bacterial stimulation and reduced the mRNA levels of Nfatc1, Ctsk, Acp5, and Oscar, but not RANKL in bone marrow-derived pre-osteoclasts. Conclusion: FTY720 inhibited proinflammatory cytokine production and suppressed osteoclastogenesis, supporting FTY720 as a potential therapy for inflammatory bone loss diseases.
MeSH term(s)	Aggregatibacter actinomycetemcomitans/physiology ; Animals ; Bone Marrow Cells/cytology ; Cytokines/metabolism ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Fingolimod Hydrochloride/pharmacology ; Gene Expression Regulation/drug effects ; Inflammation Mediators/metabolism ; Interleukin-1beta/metabolism ; Interleukin-6/metabolism ; Macrophages/drug effects ; Macrophages/metabolism ; Macrophages/microbiology ; Male ; Mice, Inbred C57BL ; Osteoclasts/drug effects ; Osteoclasts/metabolism ; Osteoclasts/microbiology ; Osteoclasts/pathology ; Osteogenesis/drug effects ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation/drug effects ; Proto-Oncogene Proteins c-akt/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism
Chemical Substances	Cytokines ; Inflammation Mediators ; Interleukin-1beta ; Interleukin-6 ; RNA, Messenger ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; Fingolimod Hydrochloride (G926EC510T)
Language	English
Publishing date	2015-07-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1476-511X
ISSN (online)	1476-511X
DOI	10.1186/s12944-015-0057-7
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Article ; Online: Sphingosine-1-phosphate signaling in vasculogenesis and angiogenesis

Kelley M Argraves / Brent A Wilkerson / W Scott Argraves

World Journal of Biological Chemistry, Vol 1, Iss 10, Pp 291-

2010 Volume 297

Abstract	Blood vessels either form de novo through the process of vasculogenesis or through angiogenesis that involves the sprouting and proliferation of endothelial cells in pre-existing blood vessels. A complex interactive network of signaling cascades downstream from at least three of the nine known G-protein-coupled sphingosine-1-phosphate (S1P) receptors act as a prime effector of neovascularization that occurs in embryonic development and in association with various pathologies. This review focuses on the current knowledge of the roles of S1P signaling in vasculogenesis and angiogenesis, with particular emphasis on vascular cell adhesion and motility responses.
Keywords	Sphingosine-1-phosphate ; Vasculogenesis ; Angiogenesis ; G-protein-coupled receptors ; Endothelium ; Biochemistry ; QD415-436 ; Organic chemistry ; QD241-441 ; Chemistry ; QD1-999 ; Science ; Q ; DOAJ:Biochemistry ; DOAJ:Life Sciences ; DOAJ:Biology and Life Sciences
Language	English
Publishing date	2010-10-01T00:00:00Z
Publisher	Baishideng Publishing
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: HDL serves as a S1P signaling platform mediating a multitude of cardiovascular effects

Argraves, Kelley M / Argraves, W. Scott

Journal of lipid research JLR. 2007 Nov., v. 48, no. 11

2007

Abstract	The lysosphingolipid sphingosine 1-phosphate (S1P) is a component of HDL. Findings from a growing number of studies indicate that S1P is a mediator of many of the cardiovascular effects of HDL, including the ability to promote vasodilation, vasoconstriction, and angiogenesis, protect against ischemia/reperfusion injury, and inhibit/reverse atherosclerosis. These latter cardioprotective effects are being shown to involve the S1P-mediated suppression of inflammatory processes, including reduction of the endothelial expression of monocyte and lymphocyte adhesion molecules, decreased recruitment of polymorphonuclear cells to sites of infarction, and blocking of cardiomyocyte apoptosis after myocardial infarction. This review article summarizes the evidence that S1P as a component of HDL serves to regulate vascular cell and lymphocyte behaviors associated with cardiovascular (patho)physiology.
Language	English
Dates of publication	2007-11
Size	p. 2325-2333.
Publishing place	American Society for Biochemistry and Molecular Biology
Document type	Article
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Cubilin maintains blood levels of HDL and albumin.

Aseem, Obaidullah / Smith, Brian T / Cooley, Marion A / Wilkerson, Brent A / Argraves, Kelley M / Remaley, Alan T / Argraves, W Scott

Journal of the American Society of Nephrology : JASN

2013 Volume 25, Issue 5, Page(s) 1028–1036

Abstract: Cubilin is an endocytic receptor highly expressed in renal proximal tubules, where it mediates uptake of albumin and filtered forms of apoA-I/HDL. Cubilin deficiency leads to urinary loss of albumin and apoA-I; however, the consequences of cubilin loss ... ...

Abstract	Cubilin is an endocytic receptor highly expressed in renal proximal tubules, where it mediates uptake of albumin and filtered forms of apoA-I/HDL. Cubilin deficiency leads to urinary loss of albumin and apoA-I; however, the consequences of cubilin loss on the homeostasis of blood albumin and apoA-I/HDL have not been studied. Using mice heterozygous for cubilin gene deletion (cubilin HT mice), we show that cubilin haploinsufficiency leads to reduced renal proximal tubular uptake of albumin and apoA-I and significantly increased urinary loss of albumin and apoA-I. Moreover, cubilin HT mice displayed significantly decreased blood levels of albumin, apoA-I, and HDL. The levels of albumin and apoA-I protein or mRNA expressed in the liver, kidney, or intestine of cubilin HT mice did not change significantly. The clearance rate of small HDL3 particles (density>1.13 g/ml) from the blood increased significantly in cubilin HT mice. In contrast, the rate of clearance of larger HDL2 particles from the blood did not change significantly, indicating a decreased half-life for HDL particles capable of filtering through the glomerulus. On the basis of these findings, we conclude that cubilin deficiency reduces renal salvage and delivery back to the blood of albumin and apoA-I, which decreases blood levels of albumin and apoA-I/HDL. These findings raise the possibility that therapeutic increase of renal cubilin expression might reduce proteinuria and increase blood levels of albumin and HDL.
MeSH term(s)	Albumins/antagonists & inhibitors ; Albumins/metabolism ; Albuminuria/etiology ; Albuminuria/genetics ; Albuminuria/metabolism ; Animals ; Apolipoprotein A-I/antagonists & inhibitors ; Apolipoprotein A-I/blood ; Apolipoprotein A-I/urine ; Gene Deletion ; Genetic Carrier Screening ; Humans ; Kidney Glomerulus/metabolism ; Kidney Glomerulus/pathology ; Lipoproteins, HDL/antagonists & inhibitors ; Lipoproteins, HDL/biosynthesis ; Lipoproteins, HDL/blood ; Lipoproteins, HDL3/antagonists & inhibitors ; Lipoproteins, HDL3/blood ; Lipoproteins, HDL3/genetics ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Receptors, Cell Surface/deficiency ; Receptors, Cell Surface/genetics ; Receptors, Cell Surface/physiology
Chemical Substances	Albumins ; Apolipoprotein A-I ; Lipoproteins, HDL ; Lipoproteins, HDL3 ; Receptors, Cell Surface ; intrinsic factor-cobalamin receptor
Language	English
Publishing date	2013-12-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2013060671
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