Junctional adhesion molecule-A, JAM-A, is a novel cell-surface marker for long-term repopulating hematopoietic stem cells

Sugano, Yasuyoshi; Takeuchi, Masaki; Hirata, Ayami; Matsushita, Hirokazu; Kitamura, Toshio; Tanaka, Minoru; Miyajima, Atsushi

doi:10.1182/blood-2007-03-081554

Cited by 52 publications

(48 citation statements)

References 48 publications

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“…Sugano et al showed that F11r was strongly expressed in the enriched HSC fraction in murine bone marrow, fetal liver, and aorta-gonad-mesonephros, and that F11r is an excellent marker for isolating HSCs. 34 These observations suggest that F11r plays important roles in the adhesion and interaction between HSCs and their niches.…”

Section: Discussionmentioning

confidence: 93%

“…30 (4) f11r (F11 receptor; also known as junctional adhesion molecule-A): F11r is a cell adhesion molecule with 2 immunoglobulin-like domains and is localized at a tight junction of epithelial, endothelial, and hematopoietic cells. [31][32][33][34] Although its role in hematopoiesis is unclear, F11r is known to play a role in the adhesion of blood cells to endothelial cells. 35 (5) 36 However, the role of Krt18 in hematopoiesis is still unknown.…”

Section: Validation Of Microarray Results By Rt-pcr and In Situ Hybrimentioning

confidence: 99%

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Comparative gene expression analysis of zebrafish and mammals identifies common regulators in hematopoietic stem cells

Kobayashi

Hiromasa

Moritomo

et al. 2010

Blood

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Hematopoiesis in teleost fish is maintained in the kidney. We previously reported that Hoechst dye efflux activity of hematopoietic stem cells (HSCs) is highly conserved in vertebrates, and that Hoechst can be used to purify HSCs from teleost kidneys. Regulatory molecules that are strongly associated with HSC activity may also be conserved in vertebrates. In this study, we identified evolutionarily conserved molecular components in HSCs by comparing the gene expression profiles of zebrafish, murine, and human HSCs. Microarray data of zebrafish kidney side population cells (zSPs) showed that genes involved in cell junction and signal transduction tended to be up-regulated in zSPs, whereas genes involved in DNA replication tended to be down-regulated. These properties of zSPs were similar to those of mammalian HSCs. Overlapping gene expression analysis showed that 40 genes were commonly up-regulated in these 3 HSCs. Some of these genes, such as egr1, gata2, and id1, have been previously implicated in the regulation of HSCs. In situ hybridization in zebrafish kidney revealed that expression domains of egr1, gata2, and id1 overlapped with that of abcg2a, a marker for zSPs. These results suggest that the overlapping genes identified in this study are regulated in HSCs and play important roles in their functions. (Blood. 2010;115: e1-e9)

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Section: Discussionmentioning

confidence: 93%

Section: Validation Of Microarray Results By Rt-pcr and In Situ Hybrimentioning

confidence: 99%

Comparative gene expression analysis of zebrafish and mammals identifies common regulators in hematopoietic stem cells

Kobayashi

Hiromasa

Moritomo

et al. 2010

Blood

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“…10 Recently, expression of several JAM family members, such as JAM-A, JAM-C, JAM4, or ESAM, has been reported in hematopoietic stem cells (HSCs), although a function for these proteins in hematopoiesis remains unknown. [11][12][13][14][15][16] In adult mammals, HSCs are rare cells mainly located in the bone marrow (BM) and able to generate all mature blood cells. In mice, HSCs are comprised within the LSK compartment as defined by the Lineage Neg c-kit Hi Sca-1 Hi (LSK) phenotype; the LSK compartment can be further subdivided using additional markers such as CD34, CD150, or CD48.…”

Section: Introductionmentioning

confidence: 99%

JAM-B regulates maintenance of hematopoietic stem cells in the bone marrow

Arcangeli

Frontera

Bardin

et al. 2011

Blood

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IntroductionThe junctional adhesion molecules (JAMs) are a subset of the immunoglobulin (Ig) protein superfamily and are characterized by the presence of both a type V and a type C2 extracellular Ig domain. JAMs and related molecules have been involved in the control of interendothelial junctions and leukocyte transendothelial migration through homotypic and heterotypic interactions. 1-5 JAM-B has been previously shown to interact with JAM-C and contributes to leukoendothelial and interendothelial cell-cell adhesion. 6,7 In mice, JAM-B expression is restricted to endothelial cells whereas JAM-C is expressed by various cell types including endothelial, 1,2 fibroblastic, 8 and smooth muscle cells. 9 Moreover, we have recently shown that JAM-C expression in lymph node fibroblastic cells is required for constitutive secretion of several chemokines such as SDF-1␣. 10 Recently, expression of several JAM family members, such as JAM-A, JAM-C, JAM4, or ESAM, has been reported in hematopoietic stem cells (HSCs), although a function for these proteins in hematopoiesis remains unknown. [11][12][13][14][15][16] In adult mammals, HSCs are rare cells mainly located in the bone marrow (BM) and able to generate all mature blood cells. In mice, HSCs are comprised within the LSK compartment as defined by the Lineage Neg c-kit Hi Sca-1 Hi (LSK) phenotype; the LSK compartment can be further subdivided using additional markers such as CD34, CD150, or CD48. Indeed, CD34 Neg CD135 Neg LSK, or Thy-1 Lo LSK 17,18 and CD150 Pos CD48 Neg LSK cells 19 have been shown to contain, respectively, around 20% and 50% of HSCs with long-term hematopoietic reconstitution potential (LT-HSCs). Because HSCs give rise to mature hematopoietic cells, including immune cells, their replacement must be adjusted to homeostatic or stress conditions such as infections, inflammation, or blood loss, and their expansion must be controlled to avoid exhaustion through inappropriate proliferation and differentiation. This is possible by the coordinated regulation of quiescence, self-renewal, and differentiation of HSCs through appropriate signals delivered by functional microenvironments called niches. [20][21][22] HSCs are restrained in these specialized microenvironments by interactions mediated by adhesion molecules and chemokine receptors expressed by HSCs, such as VLA-4 or CXCR4, with their ligands present within the BM microenvironment. Other signaling pathways controlled by growth factors and their receptors expressed on HSCs, such as angiopoietin-1 and TIE2, SCF and KIT, Thrombopoietin and MPL, have also been involved in HSC maintenance and retention in BM niches. 23,24 Whether the JAM family members expressed on HSCs also contribute to this signaling network has not been addressed so far.When necessary, HSCs enter the cell cycle to maintain BM cellularity and replenish peripheral blood in a process called mobilization, which can be induced using various hematopoietic growth factors, cyclophosphamide in combination with G-CSF (Cy/G-CSF), or intravenous inject...

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“…in the bone marrow, with their expression decreasing during the acquisition of a more differentiated state (Nagamatsu et al, 2006;Sakaguchi et al, 2006;Sugano et al, 2008;Praetor et al, 2009). Furthermore JAM-A expression has been reported to be high on undifferentiated HC11 mammary epithelial cells relative to differentiated cells (Perotti et al, 2009).…”

Section: J a M -A J A M -B J A M -C A N D J A M -4 H A V E B E E mentioning

confidence: 99%