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Article ; Online: Perspective: Hepatocyte-Directed Base Editing as Novel Treatment for Human Dyslipidemia-Current Status and Remaining Challenges.

Hoekstra, Menno / Van Eck, Miranda / Van Berkel, Theo J C

Arteriosclerosis, thrombosis, and vascular biology

2023 Volume 43, Issue 6, Page(s) 832–835

Abstract: Hyperlipidemia is a major risk factor for the development of atherosclerotic cardiovascular disease. Lipid-lowering drug therapies therefore still form the heart of the ongoing battle against the occurrence of cardiovascular events. However, in light of ... ...

Abstract	Hyperlipidemia is a major risk factor for the development of atherosclerotic cardiovascular disease. Lipid-lowering drug therapies therefore still form the heart of the ongoing battle against the occurrence of cardiovascular events. However, in light of the important improvements in gene interference and editing that have been made during the last 2 decades, gene therapy-the genetic modification of cells to produce a permanent therapeutic effect-is currently employed to relief hypercholesterolemic subjects from their potential (chronic) cardiovascular disease burden. In this perspective, we review the current status regarding hepatocyte-directed base editing to treat human dyslipidemia and provide suggestions for further technological improvement.
MeSH term(s)	Humans ; Cardiovascular Diseases/therapy ; Cardiovascular Diseases/drug therapy ; Gene Editing ; Dyslipidemias/drug therapy ; Dyslipidemias/genetics ; Hypolipidemic Agents/therapeutic use ; Hepatocytes
Chemical Substances	Hypolipidemic Agents
Language	English
Publishing date	2023-04-27
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.122.318354
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Article ; Online: N-Acetyl Galactosamine Targeting: Paving the Way for Clinical Application of Nucleotide Medicines in Cardiovascular Diseases.

Biessen, Erik A L / Van Berkel, Theo J C

Arteriosclerosis, thrombosis, and vascular biology

2021 Volume 41, Issue 12, Page(s) 2855–2865

Abstract: While the promise of oligonucleotide therapeutics, such as (chemically modified) ASO (antisense oligonucleotides) and short interfering RNAs, is undisputed from their introduction onwards, their unfavorable pharmacokinetics and intrinsic capacity to ... ...

Abstract	While the promise of oligonucleotide therapeutics, such as (chemically modified) ASO (antisense oligonucleotides) and short interfering RNAs, is undisputed from their introduction onwards, their unfavorable pharmacokinetics and intrinsic capacity to mobilize innate immune responses, were limiting widespread clinical use. However, these major setbacks have been tackled by breakthroughs in chemistry, stability and delivery. When aiming an intervention hepatic targets, such as lipid and sugar metabolism, coagulation, not to mention cancer and virus infection, introduction of N-acetylgalactosamine aided targeting technology has advanced the field profoundly and by now a dozen of N-acetylgalactosamine therapeutics for these indications have been approved for clinical use or have progressed to clinical trial stage 2 to 3 testing. This technology, in combination with major advances in oligonucleotide stability allows safe and durable intervention in targets that were previously deemed undruggable, such as Lp(a) and PCSK9 (proprotein convertase subtilisin/kexin type 9), at high efficacy and specificity, often with as little as 2 doses per year. Their successful use even the most visionary would not have predicted 2 decades ago. Here, we will review the evolution of N-acetylgalactosamine technology. We shall outline their fundamental design principles and merits, and their application for the delivery of oligonucleotide therapeutics to the liver. Finally, we will discuss the perspectives of N-acetylgalactosamine technology and propose directions for future research in receptor targeted delivery of these gene medicines.
MeSH term(s)	Acetylgalactosamine/chemistry ; Cardiovascular Diseases/drug therapy ; Drug Delivery Systems ; Genetic Therapy/methods ; Hepatocytes/drug effects ; Hepatocytes/metabolism ; Humans ; Liver/drug effects ; Liver/metabolism ; Oligonucleotides/administration & dosage ; RNAi Therapeutics
Chemical Substances	Oligonucleotides ; Acetylgalactosamine (KM15WK8O5T)
Language	English
Publishing date	2021-10-14
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.121.316290
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Article ; Online: Impact of bone marrow ATP-binding cassette transporter A1 deficiency on atherogenesis is independent of the presence of the low-density lipoprotein receptor.

Ouweneel, Amber B / Zhao, Ying / Calpe-Berdiel, Laura / Lammers, Bart / Hoekstra, Menno / Van Berkel, Theo J C / Van Eck, Miranda

Atherosclerosis

2021 Volume 319, Page(s) 79–85

Abstract: Background and aims: There is extensive evidence from bone marrow transplantation studies that hematopoietic ATP binding cassette A1 (Abca1) is atheroprotective in low-density lipoprotein receptor (Ldlr) deficient mice. In contrast, studies using ... ...

Abstract	Background and aims: There is extensive evidence from bone marrow transplantation studies that hematopoietic ATP binding cassette A1 (Abca1) is atheroprotective in low-density lipoprotein receptor (Ldlr) deficient mice. In contrast, studies using lysosyme M promoter-driven deletion of Abca1 in Ldlr deficient mice failed to show similar effects. It was hypothesized that the discrepancy between these studies might be due to the presence of Ldlr in bone marrow-derived cells in the transplantation model. In this study, we aim to determine the contribution of Ldlr to the atheroprotective effect of hematopoietic Abca1 in the murine bone marrow transplantation model. Methods: Wild-type, Ldlr Results: Bone marrow Lldr deficiency did not influence the effects of Abca1 on macrophage cholesterol efflux, foam cell formation, monocytosis or plasma cholesterol. Ldlr deficiency did reduce circulating and peritoneal lymphocyte counts, albeit only in animals lacking Abca1 in bone marrow-derived cells. Importantly, the effects of Abca1 deficiency on atherosclerosis susceptibility were unaltered by the presence or absence of Ldlr. Bone marrow Ldlr deficiency did lead to marginally but consistently decreased atherosclerosis, regardless of Abca1 deficiency. Thus, Ldlr expression on bone marrow-derived cells does, to a minimal extent, influence atherosclerotic lesion development, albeit independent of Abca1. Conclusions: This study provides novel insight into the relative impact of Ldlr and Abca1 in bone marrow-derived cells on macrophage foam cell formation and atherosclerosis development in vivo. We have shown that Ldlr and Abca1 differentially and independently influence atherosclerosis development in a murine bone marrow transplantation model of atherosclerosis.
MeSH term(s)	ATP Binding Cassette Transporter 1/genetics ; ATP-Binding Cassette Transporters/genetics ; Animals ; Atherosclerosis/genetics ; Bone Marrow/metabolism ; Cholesterol ; Lipoproteins, LDL/metabolism ; Mice ; Mice, Knockout ; Receptors, LDL/genetics ; Receptors, LDL/metabolism
Chemical Substances	ABCA1 protein, mouse ; ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters ; Lipoproteins, LDL ; Receptors, LDL ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2021-01-14
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80061-2
ISSN	1879-1484 ; 0021-9150
ISSN (online)	1879-1484
ISSN	0021-9150
DOI	10.1016/j.atherosclerosis.2021.01.001
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Article ; Online: Functionality of High-Density Lipoprotein as Antiatherosclerotic Therapeutic Target.

Hoekstra, Menno / Van Berkel, Theo J C

Arteriosclerosis, thrombosis, and vascular biology

2016 Volume 36, Issue 11, Page(s) e87–e94

MeSH term(s)	ATP Binding Cassette Transporter, Sub-Family G, Member 1/metabolism ; ATP-Binding Cassette Transporters/metabolism ; Atherosclerosis/blood ; Atherosclerosis/physiopathology ; Atherosclerosis/prevention & control ; Cardiovascular Diseases/blood ; Cardiovascular Diseases/drug therapy ; Cardiovascular Diseases/physiopathology ; Cholesterol/metabolism ; Gene Expression ; Humans ; Hypolipidemic Agents/therapeutic use ; Lipoproteins, HDL/blood ; Lipoproteins, HDL/physiology ; Macrophages/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Transcription Factors/metabolism
Chemical Substances	ABCG1 protein, human ; ATP Binding Cassette Transporter, Sub-Family G, Member 1 ; ATP-Binding Cassette Transporters ; Hypolipidemic Agents ; Lipoproteins, HDL ; MicroRNAs ; Transcription Factors ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2016-10-26
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.116.308262
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Article ; Online: ATP-binding cassette transporter A1 in lipoprotein metabolism and atherosclerosis: a new piece of the complex puzzle.

Van Eck, Miranda / Van Berkel, Theo J C

Arteriosclerosis, thrombosis, and vascular biology

2013 Volume 33, Issue 10, Page(s) 2281–2283

MeSH term(s)	ATP Binding Cassette Transporter 1/deficiency ; Animals ; Aortic Diseases/metabolism ; Atherosclerosis/metabolism ; Cholesterol/metabolism ; Female ; Liver/metabolism ; Macrophages, Peritoneal/metabolism ; Male ; Receptors, LDL/deficiency
Chemical Substances	ABCA1 protein, mouse ; ATP Binding Cassette Transporter 1 ; Receptors, LDL ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2013-10
Publishing country	United States
Document type	Comment ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.113.301719
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Article ; Online: Bringing retinoid metabolism into the 21st century.

van Berkel, Theo J C

Journal of lipid research

2009 Volume 50, Issue 12, Page(s) 2337–2339

MeSH term(s)	Animals ; Humans ; Research/trends ; Retinoids/metabolism
Chemical Substances	Retinoids
Language	English
Publishing date	2009-09-25
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
DOI	10.1194/jlr.E002659
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Article ; Online: Disruption of Phospholipid Transfer Protein-Mediated High-Density Lipoprotein Maturation Reduces Scavenger Receptor BI Deficiency-Driven Atherosclerosis Susceptibility Despite Unexpected Metabolic Complications.

Hoekstra, Menno / van der Sluis, Ronald J / Hildebrand, Reeni B / Lammers, Bart / Zhao, Ying / Praticò, Domenico / van Berkel, Theo J C / Rensen, Patrick C N / Kooijman, Sander / Jauhiainen, Matti / van Eck, Miranda

Arteriosclerosis, thrombosis, and vascular biology

2020 Volume 40, Issue 3, Page(s) 611–623

Abstract: Objective: We tested the hypothesis that enlarged, dysfunctional HDL (high-density lipoprotein) particles contribute to the augmented atherosclerosis susceptibility associated with SR-BI (scavenger receptor BI) deficiency in mice. Approach and Results: ... ...

Abstract	Objective: We tested the hypothesis that enlarged, dysfunctional HDL (high-density lipoprotein) particles contribute to the augmented atherosclerosis susceptibility associated with SR-BI (scavenger receptor BI) deficiency in mice. Approach and Results: We eliminated the ability of HDL particles to fully mature by targeting PLTP (phospholipid transfer protein) functionality. Particle size of the HDL population was almost fully normalized in male and female SR-BI×PLTP double knockout mice. In contrast, the plasma unesterified cholesterol to cholesteryl ester ratio remained elevated. The PLTP deficiency-induced reduction in HDL size in SR-BI knockout mice resulted in a normalized aortic tissue oxidative stress status on Western-type diet. Atherosclerosis susceptibility was-however-only partially reversed in double knockout mice, which can likely be attributed to the fact that they developed a metabolic syndrome-like phenotype characterized by obesity, hypertriglyceridemia, and a reduced glucose tolerance. Mechanistic studies in chow diet-fed mice revealed that the diminished glucose tolerance was probably secondary to the exaggerated postprandial triglyceride response. The absence of PLTP did not affect LPL (lipoprotein lipase)-mediated triglyceride lipolysis but rather modified the ability of VLDL (very low-density lipoprotein)/chylomicron remnants to be cleared from the circulation by the liver through receptors other than SR-BI. As a result, livers of double knockout mice only cleared 26% of the fractional dose of [ Conclusions: We have shown that disruption of PLTP-mediated HDL maturation reduces SR-BI deficiency-driven atherosclerosis susceptibility in mice despite the induction of proatherogenic metabolic complications in the double knockout mice.
MeSH term(s)	Animals ; Aorta/metabolism ; Aorta/pathology ; Atherosclerosis/blood ; Atherosclerosis/genetics ; Atherosclerosis/pathology ; Atherosclerosis/prevention & control ; Cholesterol Esters/administration & dosage ; Cholesterol Esters/blood ; Cholesterol, HDL/blood ; Disease Models, Animal ; Energy Metabolism ; Female ; Glucose Intolerance/blood ; Glucose Intolerance/genetics ; Hypertriglyceridemia/blood ; Hypertriglyceridemia/genetics ; Liver/metabolism ; Male ; Metabolic Syndrome/blood ; Metabolic Syndrome/genetics ; Mice, Inbred C57BL ; Mice, Knockout ; Obesity/blood ; Obesity/genetics ; Phospholipid Transfer Proteins/deficiency ; Phospholipid Transfer Proteins/genetics ; Plaque, Atherosclerotic ; Scavenger Receptors, Class B/deficiency ; Scavenger Receptors, Class B/genetics
Chemical Substances	Cholesterol Esters ; Cholesterol, HDL ; Phospholipid Transfer Proteins ; Scarb1 protein, mouse ; Scavenger Receptors, Class B ; phospholipid transfer protein, mouse ; cholesteryl oleate (3DPK9KFN2M)
Language	English
Publishing date	2020-01-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.119.313862
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Article ; Online: Magnetic resonance imaging contrast-enhancement with superparamagnetic iron oxide nanoparticles amplifies macrophage foam cell apoptosis in human and murine atherosclerosis.

Segers, Filip M E / Ruder, Adele V / Westra, Marijke M / Lammers, Twan / Dadfar, Seyed Mohammadali / Roemhild, Karolin / Lam, Tin Sing / Kooi, Marianne Eline / Cleutjens, Kitty B J M / Verheyen, Fons K / Schurink, Geert W H / Haenen, Guido R / van Berkel, Theo J C / Bot, Ilze / Halvorsen, Bente / Sluimer, Judith C / Biessen, Erik A L

Cardiovascular research

2022 Volume 118, Issue 17, Page(s) 3346–3359

Abstract: Aims: (Ultra) Small superparamagnetic iron oxide nanoparticles, (U)SPIO, are widely used as magnetic resonance imaging contrast media and assumed to be safe for clinical applications in cardiovascular disease. As safety tests largely relied on ... ...

Abstract	Aims: (Ultra) Small superparamagnetic iron oxide nanoparticles, (U)SPIO, are widely used as magnetic resonance imaging contrast media and assumed to be safe for clinical applications in cardiovascular disease. As safety tests largely relied on normolipidaemic models, not fully representative of the clinical setting, we investigated the impact of (U)SPIOs on disease-relevant endpoints in hyperlipidaemic models of atherosclerosis. Methods and results: RAW264.7 foam cells, exposed in vitro to ferumoxide (dextran-coated SPIO), ferumoxtran (dextran-coated USPIO), or ferumoxytol [carboxymethyl (CM) dextran-coated USPIO] (all 1 mg Fe/mL) showed increased apoptosis and reactive oxygen species accumulation for ferumoxide and ferumoxtran, whereas ferumoxytol was tolerated well. Pro-apoptotic (TUNEL+) and pro-oxidant activity of ferumoxide (0.3 mg Fe/kg) and ferumoxtran (1 mg Fe/kg) were confirmed in plaque, spleen, and liver of hyperlipidaemic ApoE-/- (n = 9/group) and LDLR-/- (n = 9-16/group) mice that had received single IV injections compared with saline-treated controls. Again, ferumoxytol treatment (1 mg Fe/kg) failed to induce apoptosis or oxidative stress in these tissues. Concomitant antioxidant treatment (EUK-8/EUK-134) largely prevented these effects in vitro (-68%, P < 0.05) and in plaques from LDLR-/- mice (-60%, P < 0.001, n = 8/group). Repeated ferumoxtran injections of LDLR-/- mice with pre-existing atherosclerosis enhanced plaque inflammation and apoptosis but did not alter plaque size. Strikingly, carotid artery plaques of endarterectomy patients who received ferumoxtran (2.6 mg Fe/kg) before surgery (n = 9) also showed five-fold increased apoptosis (18.2 vs. 3.7%, respectively; P = 0.004) compared with controls who did not receive ferumoxtran. Mechanistically, neither coating nor particle size seemed accountable for the observed cytotoxicity of ferumoxide and ferumoxtran. Conclusions: Ferumoxide and ferumoxtran, but not ferumoxytol, induced apoptosis of lipid-laden macrophages in human and murine atherosclerosis, potentially impacting disease progression in patients with advanced atherosclerosis.
MeSH term(s)	Humans ; Mice ; Animals ; Contrast Media ; Dextrans/pharmacology ; Foam Cells/pathology ; Atherosclerosis/diagnostic imaging ; Atherosclerosis/drug therapy ; Atherosclerosis/pathology ; Ferrosoferric Oxide/pharmacology ; Magnetic Resonance Imaging/methods ; Plaque, Atherosclerotic ; Macrophages/pathology ; Apoptosis ; Oxides/pharmacology
Chemical Substances	Contrast Media ; Dextrans ; Ferrosoferric Oxide (XM0M87F357) ; Oxides
Language	English
Publishing date	2022-04-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvac032
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Article ; Online: Hematopoietic arginase 1 deficiency results in decreased leukocytosis and increased foam cell formation but does not affect atherosclerosis.

Ren, Baoyan / Van Kampen, Erik / Van Berkel, Theo J C / Cruickshank, Sheena M / Van Eck, Miranda

Atherosclerosis

2017 Volume 256, Page(s) 35–46

Abstract: Background and aims: Arginase1 (Arg1), an M2 macrophage marker, plays a critical role in a number of immunological functions in macrophages, which are the main cell type facilitating atherosclerotic lesion development. Arg1 uses the substrate l-arginine ...

Abstract	Background and aims: Arginase1 (Arg1), an M2 macrophage marker, plays a critical role in a number of immunological functions in macrophages, which are the main cell type facilitating atherosclerotic lesion development. Arg1 uses the substrate l-arginine to create l-ornithine, a precursor molecule required for collagen formation and vascular smooth muscle cell differentiation. By reducing l-arginine availability, Arg1 limits the production of nitric oxide (NO), a pro-atherogenic factor in macrophages. In endothelial cells, conversely, NO is strongly anti-atherogenic. However, until now, the role of Arg1 in atherosclerosis is largely unknown. The aim of this study is to specifically investigate the effect of Arg1 deletion in hematopoietic cells on atherosclerosis susceptibility. Methods: Ldlr KO mice were transplanted with Arg1 Results: After 10-week WTD challenge, blood leukocyte counts were decreased by 25% (p < 0.001), and spleen leukocytes were decreased by 35% (p = 0.05) in Ldlr KO mice transplanted with Arg1 KO BM compared to mice transplanted with WT BM. The decrease in leukocytes was due to lower B lymphocyte counts. However, oxLDL-specific antibodies were increased in plasma of Ldlr KO mice transplanted with Arg1 KO BM compared to WT BM transplanted controls, whereas oxLDL-specific IgM was not affected. On the other hand, peritoneal foam cells in Arg1 KO BM recipients were increased 3-fold (p < 0.001) compared to WT BM recipients. No change in blood cholesterol was found. Despite changes in leukocyte counts and macrophage foam cell formation, we did not observe differences in atherosclerotic plaque size or plaque macrophage content in the aortic root. Surprisingly, there was also no difference in plaque collagen content, indicating that absence of macrophage Arg1 function does not reduce plaque stability. Conclusions: Deletion of Arg1 in hematopoietic cells adversely affects blood leukocyte counts and increases foam cell formation. However, no effects on atherosclerosis could be demonstrated, indicating that hematopoietic Arg1 function is not a decisive factor in atherosclerotic plaque formation.
MeSH term(s)	Animals ; Arginase/genetics ; Arginase/metabolism ; Atherosclerosis/blood ; Atherosclerosis/enzymology ; Atherosclerosis/genetics ; Atherosclerosis/pathology ; Bone Marrow Cells/drug effects ; Bone Marrow Cells/enzymology ; Bone Marrow Cells/pathology ; Bone Marrow Transplantation ; Cell Differentiation ; Cells, Cultured ; Cholesterol/blood ; Female ; Foam Cells/drug effects ; Foam Cells/enzymology ; Foam Cells/pathology ; Genetic Predisposition to Disease ; Leukocytes/drug effects ; Leukocytes/enzymology ; Leukocytes/pathology ; Leukocytosis/blood ; Leukocytosis/enzymology ; Leukocytosis/genetics ; Leukocytosis/prevention & control ; Lipoproteins, LDL/pharmacology ; Macrophage Activation ; Macrophages, Peritoneal/drug effects ; Macrophages, Peritoneal/enzymology ; Macrophages, Peritoneal/pathology ; Mice, Inbred C57BL ; Mice, Knockout ; Phenotype ; Plaque, Atherosclerotic ; Receptors, LDL/deficiency ; Receptors, LDL/genetics
Chemical Substances	Lipoproteins, LDL ; Receptors, LDL ; oxidized low density lipoprotein ; Cholesterol (97C5T2UQ7J) ; Arg1 protein, mouse (EC 3.5.3.1) ; Arginase (EC 3.5.3.1)
Language	English
Publishing date	2017-01
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	80061-2
ISSN	1879-1484 ; 0021-9150
ISSN (online)	1879-1484
ISSN	0021-9150
DOI	10.1016/j.atherosclerosis.2016.11.018
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Article: Peptide Antagonists for P-selectin Discriminate between Sulfatide-Dependent Platelet Aggregation and PSGL-1-Mediated Cell Adhesion.

Korporaal, Suzanne J A / Molenaar, Tom J M / Lutters, Bianca C H / Meurs, Illiana / Drost-Verhoef, Sandra / Kuiper, Johan / van Berkel, Theo J C / Biessen, Erik A L

Journal of clinical medicine

2019 Volume 8, Issue 8

Abstract: Background: Membrane-exposed sulfatides are proposed to contribute to P-selectin-dependent platelet aggregation. Here, we demonstrated that P-selectin-mediated platelet aggregation on a collagen-coated surface under flow indeed depended on sulfatides ... ...

Abstract	Background: Membrane-exposed sulfatides are proposed to contribute to P-selectin-dependent platelet aggregation. Here, we demonstrated that P-selectin-mediated platelet aggregation on a collagen-coated surface under flow indeed depended on sulfatides and that this interaction differed considerably from the interaction of P-selectin with P-selectin Glycoprotein Ligand-1 (PSGL-1), which underlies leukocyte-endothelium adhesion. Methods and results: Upon platelet activation, sulfatides were translocated to the platelet surface to form focal hot-spots. Interestingly, P-selectin was observed to exclusively interact with liposomes with a sulfatide density higher than 21% ( Conclusions: Our data suggest that the sulfatide/P-selectin interaction implicates multiple binding pockets, which only partly overlap with that of PSGL-1. These observations open ways to selectively interfere with sulfatide/P-selectin-dependent platelet aggregation without affecting PSGL-1-dependent cell adhesion.
Language	English
Publishing date	2019-08-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662592-1
ISSN	2077-0383
ISSN	2077-0383
DOI	10.3390/jcm8081266
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