CD226 is expressed on the megakaryocytic lineage from hematopoietic stem cells/progenitor cells and involved in its polyploidization

Ma, Dongchu; Sun, Yinghui; Lin, Dong; Wang, Haoyang; Dai, Bing; Zhang, Xinghai; Ouyang, Wei; Jian, Jinlong; Jia, Wei Hua; Xu, Xiaoguang; Jin, Boquan

doi:10.1111/j.1600-0609.2004.00345.x

Cited by 24 publications

(21 citation statements)

References 27 publications

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“…One of the cell‐adhesion molecules involved in polyploidization of Mk, CD226 (FLA‐1, DNAM‐1/PTA‐1), was also found highly expressed at a 5.10 ± 1.59‐fold increase in the CD41 + cells from day 10 of cultures. These observations were consistent with previous report (14).…”

Section: Discussionsupporting

confidence: 94%

Study of gene expression profile during cord blood‐associated megakaryopoiesis

Lim

Hwang

et al. 2008

European J of Haematology

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Section: Discussionsupporting

confidence: 94%

Study of gene expression profile during cord blood‐associated megakaryopoiesis

Lim

Hwang

et al. 2008

European J of Haematology

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“…81,82 Four of the other loci map in or near 4 genes that are indirectly involved in hematopoiesis in humans: jumonji gene JMJDIC, which encodes a probable histone demethylase 83 ; TPM1, which encodes tropomyosin I 84 ; SIRPA, which encodes a protein that is involved in cell adhesion 85 ; and EHD3, which encodes a mediator of protein transport and endocytosis. 86 Three other independent loci contain genes with a known influence on platelet count: BAK1 within the 6p21.3 locus encodes a proapoptotic protein that controls platelet life span 87 ; the locus at 12q24.12 harbors PTPN11, SH2B3, and BRAP, 88,89 which play a regulatory role in a wide array of cell-signaling events important in MK and other cells; and the locus at 9p24.1-p24.3 may regulate the transcription of the proximal gene JAK2, a key regulator of MK maturation, but this remains to be proved.…”

Section: Gwasmentioning

confidence: 99%

The genetics of normal platelet reactivity

Kunicki

Nugent

2010

Blood

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Genetic and environmental factors contribute to a substantial variation in platelet function seen among normal persons. Candidate gene association studies represent a valiant effort to define the genetic component in an era where genetic tools were limited, but the single nucleotide polymorphisms identified in those studies need to be validated by more objective, comprehensive approaches, such as genome-wide association studies (GWASs) of quantitative functional traits in much larger cohorts of more carefully selected normal subjects. During the past year, platelet count and mean platelet volume, which indirectly affect platelet function, were the subjects of GWAS. IntroductionInterindividual platelet responsiveness to a variety of agonists is highly variable, as documented in several studies of large cohorts of normal persons. [1][2][3][4][5][6][7][8][9][10][11][12] At the same time, these and other studies of siblings, twins, and families with a history of coronary artery disease (CAD) have documented that intraindividual responsiveness is highly reproducible over time, regardless of the agonist tested or the chosen method of assessment. These findings strongly suggest that there is a high level of heritability of platelet function, and this has prompted numerous attempts to define the genetic basis for platelet function variability. A summary of platelet functionTo fully appreciate the gene association studies, it is necessary to briefly summarize key aspects of platelet function and establish a molecular and physiologic basis for the selection of genes to study.When a blood vessel is damaged, circulating platelets interact with components of the extracellular matrix, particularly collagen, and a complex series of receptor-ligand interactions ensues that ultimately leads to the formation of a stable platelet plug or thrombus. This process is a continuum of at least 3 phases that we can describe as initiation, extension, and consolidation, each of which entails the cooperation of a different group of receptors.In the initiation phase, plasma von Willebrand factor (VWF) binds to collagen via its A3 domain and becomes structurally altered such that its A1 domain then binds to the platelet membrane receptor glycoprotein Ib-IX-V complex (GPIb complex). It is the GPIb␣ or larger subunit of GPIb that makes direct contact with VWF. This association is a requisite step in the adhesion of platelets to exposed thrombogenic surfaces at sites of vessel wall injury or in regions of atherosclerotic plaque rupture. Concurrently, a more stable platelet monolayer is formed on the collagen surface mediated predominantly by the platelet-specific receptor glycoprotein VI (GPVI) and platelet integrin ␣ 2 ␤ 1 .The engagement of these receptors enhances platelet activation leading to the extension phase, mediated largely by the conversion of prothrombin to thrombin at the activated platelet surface and the secretion of active compounds from platelet granules (␣-granules and ␦-granules), which can further stimulate platelets. One of...

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“…CD226, a type I transmembrane receptor of the immunoglobulin superfamily that has 2 immunoglobulin‐like extracellular domains, is predominantly expressed on the surface of T cells and NK cells and is also present on monocytes, platelets, a subset of B cells (3), mast cells (8), and megakaryocytes (9). CD226 is involved in the activation and differentiation of T cells (10–12), adhesion and cytotoxicity of T cells and NK cells (3, 13), apoptosis (7, 14), transendothelial migration of monocytes (15), and activation and aggregation of platelets (16, 17).…”

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confidence: 99%

A 3′‐untranslated region variant is associated with impaired expression of CD226 in T and natural killer T cells and is associated with susceptibility to systemic lupus erythematosus

Löfgren¹,

Delgado-Vega²,

Gallant³

et al. 2010

Arthritis & Rheumatism

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Objective. Costimulatory receptor CD226 plays an important role in T cell activation, differentiation, and cytotoxicity. This study was undertaken to investigate the genetic association of CD226 with susceptibility to systemic lupus erythematosus (SLE) and to assess the functional implications of this association.Methods. Twelve tag single-nucleotide polymorphisms (SNPs) in CD226 were typed in 1,163 SLE patients and 1,482 healthy control subjects from Europe or of European ancestry. Analyses of association were performed by single-marker Cochran-Mantel-Haenszel meta-analysis, followed by haplotype analysis. Gene expression was analyzed by quantitative real-time polymerase chain reaction analyses of RNA from peripheral blood mononuclear cells, and by fluorescence-activated cell sorter analysis. To study the functional impact of the associated variants, luciferase reporter constructs containing different portions of the 3-untranslated

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CD226 is expressed on the megakaryocytic lineage from hematopoietic stem cells/progenitor cells and involved in its polyploidization

Abstract: CD226 molecules play an important role in maturation of the megakaryocytes in combination with LFA-1.

Cited by 24 publications

References 27 publications

Study of gene expression profile during cord blood‐associated megakaryopoiesis

Study of gene expression profile during cord blood‐associated megakaryopoiesis

The genetics of normal platelet reactivity

A 3′‐untranslated region variant is associated with impaired expression of CD226 in T and natural killer T cells and is associated with susceptibility to systemic lupus erythematosus

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