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• W3007242593 abstract "Monocyte rolling, adhesion, and transmigration across the endothelium are mediated by specific interactions between surface adhesion molecules. This process is fundamental to innate immunity and to inflammatory disease, including atherosclerosis, where monocyte egress into the intimal space is central to formation of fatty plaques. Monocytes are a heterogeneous population of three distinct subsets of cells, all of which play different roles in atherosclerosis progression. However, it is not well understood how interactions between different monocyte subsets and the endothelium are regulated. Furthermore, it is appreciated that endothelial adhesion molecules are heavily N-glycosylated, but beyond regulating protein trafficking to the cell surface, whether and if so how these N-glycans contribute to monocyte recruitment is not known. This review discusses how changes in endothelial N-glycosylation may impact vascular and monocytic inflammation. It will also discuss how regulating N-glycoforms on the endothelial surface may allow for the recruitment of specific monocyte subsets to sites of inflammation, and how further understanding in this area may lead to the development of glyco-specific therapeutics in the treatment of cardiovascular disease. Monocyte rolling, adhesion, and transmigration across the endothelium are mediated by specific interactions between surface adhesion molecules. This process is fundamental to innate immunity and to inflammatory disease, including atherosclerosis, where monocyte egress into the intimal space is central to formation of fatty plaques. Monocytes are a heterogeneous population of three distinct subsets of cells, all of which play different roles in atherosclerosis progression. However, it is not well understood how interactions between different monocyte subsets and the endothelium are regulated. Furthermore, it is appreciated that endothelial adhesion molecules are heavily N-glycosylated, but beyond regulating protein trafficking to the cell surface, whether and if so how these N-glycans contribute to monocyte recruitment is not known. This review discusses how changes in endothelial N-glycosylation may impact vascular and monocytic inflammation. It will also discuss how regulating N-glycoforms on the endothelial surface may allow for the recruitment of specific monocyte subsets to sites of inflammation, and how further understanding in this area may lead to the development of glyco-specific therapeutics in the treatment of cardiovascular disease. The endothelium, via a myriad of mechanisms, orchestrates vascular homeostasis to maintain a healthy luminal surface. Perturbation of these mechanisms, as occurs by chronic exposure of the endothelial cell layer to hyperlipidemia, hyperglycemia, pro-oxidant and inflammatory stimuli, or turbulent blood flow, results in endothelial dysfunction. The latter is an established feature of vascular inflammatory disease, including atherosclerosis, a chronic disease that leads to the buildup of fat-filled plaques in the vessel wall.1Aird W.C. Phenotypic heterogeneity of the endothelium, II: representative vascular beds.Circ Res. 2007; 100: 174-190Crossref PubMed Scopus (778) Google Scholar, 2Cejkova S. Kralova-Lesna I. Poledne R. Monocyte adhesion to the endothelium is an initial stage of atherosclerosis development.Cor Vasa. 2015; 58: e419-e425Crossref Scopus (52) Google Scholar, 3Esper R.J. Nordaby R.A. Vilarino J.O. Paragano A. Cacharron J.L. Machado R.A. Endothelial dysfunction: a comprehensive appraisal.Cardiovasc Diabetol. 2006; 5: 4Crossref PubMed Scopus (348) Google Scholar A dysfunctional endothelium is characterized by various biochemical, morphologic, molecular, and functional changes. Cardinal among these is a more adhesive endothelial surface, which, in turn, is key to the recruitment and extravasation of monocytes into the subendothelial space.2Cejkova S. Kralova-Lesna I. Poledne R. Monocyte adhesion to the endothelium is an initial stage of atherosclerosis development.Cor Vasa. 2015; 58: e419-e425Crossref Scopus (52) Google Scholar Circulating monocytes are captured onto the endothelium via a process of rolling, firm adhesion, and ultimately migration through the endothelium to the intima, after which they can differentiate into macrophages and form fatty plaque formation. Specific binding between adhesion molecules expressed on the surface of the leukocyte and endothelium is the established mechanism by which monocytes roll, adhere, and transmigrate across the endothelium. These adhesion molecules, their respective cognate receptors, and their roles in the adhesion cascade are known and how their function is controlled is also largely understood. On the endothelial side, the most appreciated mechanism involves regulation of surface adhesion molecule expression levels. Proinflammatory stimuli induce signaling cascades, typically via NF-κB, that either up-regulate gene, protein, and then surface expression, and/or mobilize preformed intracellular stores of adhesion molecules to the cell surface, where they can interact with circulating leukocytes.4Devaux B. Scholz D. Hirche A. Klovekorn W.P. Schaper J. Upregulation of cell adhesion molecules and the presence of low grade inflammation in human chronic heart failure.Eur Heart J. 1997; 18: 470-479Crossref PubMed Scopus (234) Google Scholar,5Rondaij M.G. Bierings R. Kragt A. van Mourik J.A. Voorberg J. Dynamics and plasticity of Weibel-Palade bodies in endothelial cells.Arterioscler Thromb Vasc Biol. 2006; 26: 1002-1007Crossref PubMed Scopus (263) Google Scholar Strategies that target and inhibit endothelial adhesion molecule function, although effective in cell and preclinical models, have not translated to the clinic.6Haverslag R. Pasterkamp G. Hoefer I. Targeting adhesion molecules in cardiovascular disorders.Cardiovasc Hematol Disord Drug Targets. 2008; 8: 252-260Crossref PubMed Scopus (45) Google Scholar Furthermore, much of our knowledge of endothelial adhesion molecule function, and how they bind with their cognate receptors on the monocyte, was elucidated at a time when both monocyte and vascular endothelial heterogeneity were not as appreciated as they are now. For example, monocytes exist in at least three distinct subtypes, each with varying functions in disease pathogenesis.7Boyette L.B. Macedo C. Hadi K. Elinoff B.D. Walters J.T. Ramaswami B. Chalasani G. Taboas J.M. Lakkis F.G. Metes D.M. Phenotype, function, and differentiation potential of human monocyte subsets.PLoS One. 2017; 12: e0176460Crossref PubMed Scopus (205) Google Scholar,8Swirski F.K. Weissleder R. Pittet M.J. Heterogeneous in vivo behavior of monocyte subsets in atherosclerosis.Arterioscler Thromb Vasc Biol. 2009; 29: 1424-1432Crossref PubMed Scopus (115) Google Scholar Moreover, the mechanisms governing endothelial responses to inflammation vary, depending on the vascular bed in which these cells reside.1Aird W.C. Phenotypic heterogeneity of the endothelium, II: representative vascular beds.Circ Res. 2007; 100: 174-190Crossref PubMed Scopus (778) Google Scholar,9Aird W.C. Endothelial cell heterogeneity.Cold Spring Harb Perspect Med. 2012; 2: a006429Crossref PubMed Scopus (460) Google Scholar These newer insights collectively highlight, in our opinion, a poorly understood aspect of monocyte-endothelial interactions (namely, are there different mechanisms that regulate how different monocyte subsets adhere to the endothelium, and in a manner that allows vascular bed and/or disease selectivity?). If so, how do these mechanisms change during the transition from innate immune responses to inflammatory disease? This review discusses the concept of an endothelial zip code (ie, that there are molecular and/or biochemical signatures across vascular beds that control the homing of monocyte subsets to specific endothelial surfaces).1Aird W.C. Phenotypic heterogeneity of the endothelium, II: representative vascular beds.Circ Res. 2007; 100: 174-190Crossref PubMed Scopus (778) Google Scholar,9Aird W.C. Endothelial cell heterogeneity.Cold Spring Harb Perspect Med. 2012; 2: a006429Crossref PubMed Scopus (460) Google Scholar,10Renkonen J. Tynninen O. Hayry P. Paavonen T. Renkonen R. Glycosylation might provide endothelial zip codes for organ-specific leukocyte traffic into inflammatory sites.Am J Pathol. 2002; 161: 543-550Abstract Full Text Full Text PDF PubMed Scopus (81) Google Scholar This discussion is focused on endothelial adhesion molecule N-glycosylation, a post-translational modification that remains a relatively underexplored facet of the mechanisms regulating adhesion molecule function. Studies have shown that N-glycosylation of these proteins is a regulated process during inflammation, with this regulation varying depending on the vascular bed of origin or disease process (eg, cardiovascular, metabolic, or cancer).11Scott D.W. Vallejo M.O. Patel R.P. Heterogenic endothelial responses to inflammation: role for differentital N-glycosylation and vascular bed of origin.J Am Heart Assoc. 2013; 2: e000263Crossref PubMed Scopus (49) Google Scholar,12de Leoz M.L. Young L.J. An H.J. Kronewitter S.R. Kim J. Miyamoto S. Borowsky A.D. Chew H.K. Lebrilla C.B. High-mannose glycans are elevated during breast cancer progression.Mol Cell Proteomics. 2011; 10 (M110.002717)Crossref PubMed Google Scholar Regulation in this context does not refer to the binary, presence or absence of N-glycosylation per se, as is the case with other post-translational modifications (eg, phosphorylation), but instead refers to the changing composition of sugars within the N-glycan structure. Within this framework, we discuss the current understanding, hypotheses, and questions regarding how inflammation regulates endothelial N-glycosylation, giving rise to different N-glycoforms of the same adhesion molecule(s), and subsequently an endothelial N-glycan zip code that is critical to selective recruitment of monocyte subsets. This review also discusses how specific adhesion molecule N-glycoforms may offer new targets to therapeutically modulate monocyte-endothelial interactions in inflammatory disease, but not innate immune processes. Monocytes are myeloid-derived cells integral to the innate immune system and make up 5% to 10% of total circulating leukocytes in healthy adults. Once mature and released from the bone marrow, they circulate for several days before undergoing cell death or infiltrating injured tissues, where they differentiate into macrophages and dendritic cells to resolve inflammation.13van Furth R. Raeburn J.A. van Zwet T.L. Characteristics of human mononuclear phagocytes.Blood. 1979; 54: 485-500Crossref PubMed Google Scholar Human monocytes are categorized into three different subsets based on surface expression of the lipopolysaccharide receptor CD14 and the Fcγ receptor III CD16. In healthy adults, approximately 90% of circulating human monocytes are classical monocytes (CD14++/CD16−) with the remaining approximately 10% comprising nonclassical (CD14+/CD16++) and intermediate (CD14++/CD16+) monocytes.7Boyette L.B. Macedo C. Hadi K. Elinoff B.D. Walters J.T. Ramaswami B. Chalasani G. Taboas J.M. Lakkis F.G. Metes D.M. Phenotype, function, and differentiation potential of human monocyte subsets.PLoS One. 2017; 12: e0176460Crossref PubMed Scopus (205) Google Scholar,14Ziegler-Heitbrock L. Blood monocytes and their subsets: established features and open questions.Front Immunol. 2015; 6: 423Crossref PubMed Scopus (179) Google Scholar Of the three subsets, classical monocytes are considered anti-inflammatory due to having the highest production levels of IL-10.15Idzkowska E. Eljaszewicz A. Miklasz P. Musial W.J. Tycinska A.M. Moniuszko M. The role of different monocyte subsets in the pathogenesis of atherosclerosis and acute coronary syndromes.Scand J Immunol. 2015; 82: 163-173Crossref PubMed Scopus (65) Google Scholar They have high expression of genes encoding phagocytic, antimicrobial, and wound healing activities, highlighting their importance in tissue repair.16Cros J. Cagnard N. Woollard K. Patey N. Zhang S.Y. Senechal B. Puel A. Biswas S.K. Moshous D. Picard C. Jais J.P. D'Cruz D. Casanova J.L. Trouillet C. Geissmann F. Human CD14dim monocytes patrol and sense nucleic acids and viruses via TLR7 and TLR8 receptors.Immunity. 2010; 33: 375-386Abstract Full Text Full Text PDF PubMed Scopus (875) Google Scholar, 17Smedman C. Ernemar T. Gudmundsdotter L. Gille-Johnson P. Somell A. Nihlmark K. Gardlund B. Andersson J. Paulie S. FluoroSpot analysis of TLR-activated monocytes reveals several distinct cytokine-secreting subpopulations.Scand J Immunol. 2012; 75: 249-258Crossref PubMed Scopus (25) Google Scholar, 18Zawada A.M. Rogacev K.S. Rotter B. Winter P. Marell R.R. Fliser D. Heine G.H. SuperSAGE evidence for CD14++CD16+ monocytes as a third monocyte subset.Blood. 2011; 118: e50-e61Crossref PubMed Scopus (375) Google Scholar Nonclassical monocytes express genes associated with cytoskeletal rearrangement, allowing for their patrolling behavior along the endothelium to survey tissues.19Auffray C. Fogg D. Garfa M. Elain G. Join-Lambert O. Kayal S. Sarnacki S. Cumano A. Lauvau G. Geissmann F. Monitoring of blood vessels and tissues by a population of monocytes with patrolling behavior.Science. 2007; 317: 666-670Crossref PubMed Scopus (1357) Google Scholar,20Wong K.L. Tai J.J. Wong W.C. Han H. Sem X. Yeap W.H. Kourilsky P. Wong S.C. Gene expression profiling reveals the defining features of the classical, intermediate, and nonclassical human monocyte subsets.Blood. 2011; 118: e16-e31Crossref PubMed Scopus (649) Google Scholar They also have little secretory activity, only triggered by viruses or nucleic acids.16Cros J. Cagnard N. Woollard K. Patey N. Zhang S.Y. Senechal B. Puel A. Biswas S.K. Moshous D. Picard C. Jais J.P. D'Cruz D. Casanova J.L. Trouillet C. Geissmann F. Human CD14dim monocytes patrol and sense nucleic acids and viruses via TLR7 and TLR8 receptors.Immunity. 2010; 33: 375-386Abstract Full Text Full Text PDF PubMed Scopus (875) Google Scholar Intermediate monocytes fall on a middle ground between the classical and nonclassical types. They have the greatest inflammatory potential and are the greatest producers of reactive oxygen species, for example.16Cros J. Cagnard N. Woollard K. Patey N. Zhang S.Y. Senechal B. Puel A. Biswas S.K. Moshous D. Picard C. Jais J.P. D'Cruz D. Casanova J.L. Trouillet C. Geissmann F. Human CD14dim monocytes patrol and sense nucleic acids and viruses via TLR7 and TLR8 receptors.Immunity. 2010; 33: 375-386Abstract Full Text Full Text PDF PubMed Scopus (875) Google Scholar,18Zawada A.M. Rogacev K.S. Rotter B. Winter P. Marell R.R. Fliser D. Heine G.H. SuperSAGE evidence for CD14++CD16+ monocytes as a third monocyte subset.Blood. 2011; 118: e50-e61Crossref PubMed Scopus (375) Google Scholar,21Rossol M. Kraus S. Pierer M. Baerwald C. Wagner U. The CD14(bright) CD16+ monocyte subset is expanded in rheumatoid arthritis and promotes expansion of the Th17 cell population.Arthritis Rheum. 2012; 64: 671-677Crossref PubMed Scopus (250) Google Scholar,22Belge K.U. Dayyani F. Horelt A. Siedlar M. Frankenberger M. Frankenberger B. Espevik T. Ziegler-Heitbrock L. The proinflammatory CD14+CD16+DR++ monocytes are a major source of TNF.J Immunol. 2002; 168: 3536-3542Crossref PubMed Scopus (673) Google Scholar They harbor the highest expression of major histocompatibility complex-II (human leukocyte antigen-DR), which, in turn, gives them a strong capability of inducing CD4+ T-cell proliferation.15Idzkowska E. Eljaszewicz A. Miklasz P. Musial W.J. Tycinska A.M. Moniuszko M. The role of different monocyte subsets in the pathogenesis of atherosclerosis and acute coronary syndromes.Scand J Immunol. 2015; 82: 163-173Crossref PubMed Scopus (65) Google Scholar,20Wong K.L. Tai J.J. Wong W.C. Han H. Sem X. Yeap W.H. Kourilsky P. Wong S.C. Gene expression profiling reveals the defining features of the classical, intermediate, and nonclassical human monocyte subsets.Blood. 2011; 118: e16-e31Crossref PubMed Scopus (649) Google Scholar In contrast, some studies have demonstrated that intermediate monocytes are robust producers of the anti-inflammatory cytokine, IL-10.23Skrzeczynska-Moncznik J. Bzowska M. Loseke S. Grage-Griebenow E. Zembala M. Pryjma J. Peripheral blood CD14 high CD16+ monocytes are main producers of IL-10.Scand J Immunol. 2008; 67: 152-159Crossref PubMed Scopus (219) Google Scholar,24Shantsila E. Wrigley B. Tapp L. Apostolakis S. Montoro-Garcia S. Drayson M.T. Lip G.Y. Immunophenotypic characterization of human monocyte subsets: possible implications for cardiovascular disease pathophysiology.J Thromb Haemost. 2011; 9: 1056-1066Crossref PubMed Scopus (135) Google Scholar This speaks to the true intermediate nature of these monocytes; however, in the context of disease, it seems that the proinflammatory function of intermediate monocytes dominates any anti-inflammatory capabilities, as will be discussed further in this review. Monocytes are key contributors to atherosclerotic plaque development, as they differentiate into macrophages in the intima that provide foci for foam cell formation.25Nahrendorf M. Myeloid cell contributions to cardiovascular health and disease.Nat Med. 2018; 24: 711-720Crossref PubMed Scopus (133) Google Scholar,26Randolph G.J. The fate of monocytes in atherosclerosis.J Thromb Haemost. 2009; 7 Suppl 1: 28-30Crossref PubMed Scopus (45) Google Scholar As monocytes contribute to both initial lesion formation and lesion advancement,27Babaev V.R. Bobryshev Y.V. Sukhova G.K. Kasantseva I.A. Monocyte/macrophage accumulation and smooth muscle cell phenotypes in early atherosclerotic lesions of human aorta.Atherosclerosis. 1993; 100: 237-248Abstract Full Text PDF PubMed Scopus (54) Google Scholar, 28Bobryshev Y.V. Monocyte recruitment and foam cell formation in atherosclerosis.Micron. 2006; 37: 208-222Crossref PubMed Scopus (269) Google Scholar, 29Bobryshev Y.V. Lord R.S. Ultrastructural recognition of cells with dendritic cell morphology in human aortic intima: contacting interactions of vascular dendritic cells in athero-resistant and athero-prone areas of the normal aorta.Arch Histol Cytol. 1995; 58: 307-322Crossref PubMed Scopus (168) Google Scholar, 30Libby P. Changing concepts of atherogenesis.J Intern Med. 2000; 247: 349-358Crossref PubMed Scopus (519) Google Scholar, 31Lusis A.J. Atherosclerosis.Nature. 2000; 407: 233-241Crossref PubMed Scopus (4668) Google Scholar understanding the dynamics of monocyte adhesion to endothelial cells remains an important question in understanding the proinflammatory mechanisms underlying atherogenesis. Specific monocyte subsets are associated with distinct stages and disease outcomes. Multiple studies have demonstrated that circulating intermediate monocytes correlate with more advanced atherosclerosis and peripheral artery disease, and independently predict adverse cardiac events in at-risk patients.21Rossol M. Kraus S. Pierer M. Baerwald C. Wagner U. The CD14(bright) CD16+ monocyte subset is expanded in rheumatoid arthritis and promotes expansion of the Th17 cell population.Arthritis Rheum. 2012; 64: 671-677Crossref PubMed Scopus (250) Google Scholar,32Rogacev K.S. Cremers B. Zawada A.M. Seiler S. Binder N. Ege P. Grosse-Dunker G. Heisel I. Hornof F. Jeken J. Rebling N.M. Ulrich C. Scheller B. Bohm M. Fliser D. Heine G.H. CD14++CD16+ monocytes independently predict cardiovascular events: a cohort study of 951 patients referred for elective coronary angiography.J Am Coll Cardiol. 2012; 60: 1512-1520Crossref PubMed Scopus (385) Google Scholar, 33Wildgruber M. Aschenbrenner T. Wendorff H. Czubba M. Glinzer A. Haller B. Schiemann M. Zimmermann A. Berger H. Eckstein H.H. Meier R. Wohlgemuth W.A. Libby P. Zernecke A. The “intermediate” CD14(++)CD16(+) monocyte subset increases in severe peripheral artery disease in humans.Sci Rep. 2016; 6: 39483Crossref PubMed Scopus (57) Google Scholar, 34Heine G.H. Ulrich C. Seibert E. Seiler S. Marell J. Reichart B. Krause M. Schlitt A. Kohler H. Girndt M. CD14(++)CD16+ monocytes but not total monocyte numbers predict cardiovascular events in dialysis patients.Kidney Int. 2008; 73: 622-629Abstract Full Text Full Text PDF PubMed Scopus (178) Google Scholar, 35Merino A. Buendia P. Martin-Malo A. Aljama P. Ramirez R. Carracedo J. Senescent CD14+CD16+ monocytes exhibit proinflammatory and proatherosclerotic activity.J Immunol. 2011; 186: 1809-1815Crossref PubMed Scopus (129) Google Scholar, 36Berg K.E. Ljungcrantz I. Andersson L. Bryngelsson C. Hedblad B. Fredrikson G.N. Nilsson J. Bjorkbacka H. Elevated CD14++CD16- monocytes predict cardiovascular events.Circ Cardiovasc Genet. 2012; 5: 122-131Crossref PubMed Scopus (181) Google Scholar Results from the HOM SWEET HOMe32Rogacev K.S. Cremers B. Zawada A.M. Seiler S. Binder N. Ege P. Grosse-Dunker G. Heisel I. Hornof F. Jeken J. Rebling N.M. Ulrich C. Scheller B. Bohm M. Fliser D. Heine G.H. CD14++CD16+ monocytes independently predict cardiovascular events: a cohort study of 951 patients referred for elective coronary angiography.J Am Coll Cardiol. 2012; 60: 1512-1520Crossref PubMed Scopus (385) Google Scholar and the CARE FOR HOMe37Zawada A.M. Fell L.H. Untersteller K. Seiler S. Rogacev K.S. Fliser D. Ziegler-Heitbrock L. Heine G.H. Comparison of two different strategies for human monocyte subsets gating within the large-scale prospective CARE FOR HOMe Study.Cytometry A. 2015; 87: 750-758Crossref PubMed Scopus (29) Google Scholar studies show positive correlations between the levels of intermediate monocyte subsets with disease severity, prevalence of adverse cardiac events, and cardiac-related mortality in patients at risk for cardiovascular disease and in chronic kidney disease patients. In both of these studies, large cohorts of patients at increased cardiovascular risk were followed up for 3 to 4 years, and after adjustments for confounders, both studies found that intermediate monocytes were the only subset to independently correlate with cardiovascular events in these at-risk patient populations.32Rogacev K.S. Cremers B. Zawada A.M. Seiler S. Binder N. Ege P. Grosse-Dunker G. Heisel I. Hornof F. Jeken J. Rebling N.M. Ulrich C. Scheller B. Bohm M. Fliser D. Heine G.H. CD14++CD16+ monocytes independently predict cardiovascular events: a cohort study of 951 patients referred for elective coronary angiography.J Am Coll Cardiol. 2012; 60: 1512-1520Crossref PubMed Scopus (385) Google Scholar,34Heine G.H. Ulrich C. Seibert E. Seiler S. Marell J. Reichart B. Krause M. Schlitt A. Kohler H. Girndt M. CD14(++)CD16+ monocytes but not total monocyte numbers predict cardiovascular events in dialysis patients.Kidney Int. 2008; 73: 622-629Abstract Full Text Full Text PDF PubMed Scopus (178) Google Scholar,37Zawada A.M. Fell L.H. Untersteller K. Seiler S. Rogacev K.S. Fliser D. Ziegler-Heitbrock L. Heine G.H. Comparison of two different strategies for human monocyte subsets gating within the large-scale prospective CARE FOR HOMe Study.Cytometry A. 2015; 87: 750-758Crossref PubMed Scopus (29) Google Scholar These data may be explained by selective recruitment of nonclassical/intermediate CD16+ monocytes, over classical CD16− monocytes, to inflamed endothelial cells. An important consideration in understanding how monocytes adhere is their relative cell numbers; greater numbers increase probability of adhesion by the law of mass action. Indeed, in atherosclerosis, total monocyte numbers are increased, but relative distribution between classical and nonclassical is shifted; CD16+ monocytes can expand to approximately 20% to 30% of the total monocyte population, whereas CD16− monocyte levels can decrease to approximately 70% to 80%.32Rogacev K.S. Cremers B. Zawada A.M. Seiler S. Binder N. Ege P. Grosse-Dunker G. Heisel I. Hornof F. Jeken J. Rebling N.M. Ulrich C. Scheller B. Bohm M. Fliser D. Heine G.H. CD14++CD16+ monocytes independently predict cardiovascular events: a cohort study of 951 patients referred for elective coronary angiography.J Am Coll Cardiol. 2012; 60: 1512-1520Crossref PubMed Scopus (385) Google Scholar,34Heine G.H. Ulrich C. Seibert E. Seiler S. Marell J. Reichart B. Krause M. Schlitt A. Kohler H. Girndt M. 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• W3007242593 created "2020-03-06" @default.
• W3007242593 creator A5021751784 @default.
• W3007242593 creator A5091117546 @default.
• W3007242593 date "2020-05-01" @default.
• W3007242593 modified "2023-09-29" @default.
• W3007242593 title "Selective Recruitment of Monocyte Subsets by Endothelial N-Glycans" @default.
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