Endothelial selectins and vascular cell adhesion molecule-1 promote hematopoietic progenitor homing to bone marrow

Frenette, Paul S.; Subbarao, Sangeetha; Mazo, Irina B.; Andrian, Ulrich H. von; Wagner, Denisa D.

doi:10.1073/pnas.95.24.14423

Cited by 355 publications

(286 citation statements)

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“…[23][24][25] In this context, the role of different integrin subfamilies is currently under intensive investigation. 26,27 With respect to non-marrow organs, extensive studies have been performed on mature Stem cell adhesion requires eNOS A Kaminski et al leukocyte behavior, 28,29 but there are few reports on peripheral stem cell-endothelium interactions in vivo.…”

Section: Discussionmentioning

confidence: 99%

Endothelial NOS is required for SDF-1α/CXCR4-mediated peripheral endothelial adhesion of c-kit+ bone marrow stem cells

Kaminski

Donndorf

et al. 2008

Laboratory Investigation

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In the era of intravascular approaches for regenerative cell therapy, the underlying mechanisms of stem cell migration to non-marrow tissue have not been clarified. We hypothesized that next to a local inflammatory response implying adhesion molecule expression, endothelial nitric oxide synthase (eNOS)-dependent signaling is required for stromalcell-derived factor-1 alpha (SDF-1a)-induced adhesion of c-kit þ cells to the vascular endothelium. SDF-1a/tumor necrosis factor-alpha (TNF-a)-induced c-kit þ -cell shape change and migration capacity was studied in vitro using immunohistochemistry and Boyden chamber assays. In vivo interaction of c-kit þ cells from bone marrow with the endothelium in response to SDF-1a/TNF-a stimulation was visualized in the cremaster muscle microcirculation of wild-type (WT) and eNOS (À/À) mice using intravital fluorescence microscopy. In addition, NOS activity was inhibited with N-nitro-Larginine-methylester-hydrochloride in WT mice. To reveal c-kit þ -specific adhesion behavior, endogenous leukocytes (EL) and c-kit þ cells from peripheral blood served as control. Moreover, intercellular adhesion molecule-1 (ICAM-1) and CXCR4 were blocked systemically to determine their role in inflammation-related c-kit þ -cell adhesion. In vitro, SDF-1a enhanced c-kit þ -cell migration. In vivo, SDF-1a alone triggered endothelial rolling-not firm adherence-of c-kit þ cells in WT mice. While TNF-a alone had little effect on adhesion of c-kit þ cells, it induced maximum endothelial EL adherence. However, after combined treatment with SDF-1a þ TNF-a, endothelial adhesion of c-kit þ cells increased independent of their origin, while EL adhesion was not further incremented. Systemic treatment with anti-ICAM-1 and anti-CXCR4-monoclonal antibody completely abolished endothelial c-kit þ -cell adhesion. In N-nitro-L-arginine-methylester-hydrochloride-treated WT mice as well as in eNOS (À/À) mice, firm endothelial adhesion of c-kit þ cells was entirely abrogated, while EL adhesion was significantly increased. The chemokine SDF-1a mediates firm adhesion c-kit þ cells only in the presence of TNF-a stimulation via an ICAM-1-and CXCR4-dependent mechanism. The presence of eNOS appears to be a crucial and specific factor for firm c-kit þ -cell adhesion to the vascular endothelium.

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Section: Discussionmentioning

confidence: 99%

Endothelial NOS is required for SDF-1α/CXCR4-mediated peripheral endothelial adhesion of c-kit+ bone marrow stem cells

Kaminski

Donndorf

et al. 2008

Laboratory Investigation

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“…Plates were scored on a dissecting microscope for high-proliferative potential colony-forming cells (HPP-CFC, highly dense colonies >0.5 mm in diameter) (Bradley and Hodgson, 1979). Frenette et al (1998) used a surrogate assay to evaluate the progenitor potential of homed whole bone marrow cells. In our experiments, B6.SJL (Ly5.1) whole bone marrow cells (100 × 10 6 ) were injected into lethally irradiated BALB/c mice (10 Gy).…”

Section: Hpp-cfc In Vitro Progenitor Assaymentioning

confidence: 99%

“…Using syngeneic inbred mice, many aspects of stem cell homing have been described (Vos et al, 1980;Visser and Eliason, 1983;Bertoncello et al, 1985;Tavassoli and Aizawa, 1987;Hardy et al, 1991;Hendrikx et al, 1996;Nilsson et al, 1996;Nibley et al, 1997;Shaaban et al, 1999;Lanzkron et al, 1999a;Askenasy et al, 2003). The process involves rapid phenotypic changes in the infused stem cells and the interactions of multiple adhesion protein and their receptors (Papayannopoulou and Craddock, 1997;Frenette et al, 1998;Becker et al, 1999;Lapidot et al, 2005). Marrow stem cells enter S phase within about 12 h after infusion in vivo.…”

mentioning

confidence: 99%

Murine allogeneic in vivo stem cell homing^,

Colvin

Lambert²,

Dooner

et al. 2006

Journal Cellular Physiology

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Stem cell homing has been studied in syngeneic models and appears to be rapid (<1 h) and dependent on cellular adhesion and migration factors. We utilized a full H2-mismatched transplantation model to determine the basics of allogeneic homing. C57BL/6J Lin-Sca-1+ cells were labeled with CFSE and injected in non-myeloablated BALB/c mice. Fluorescent cell detection was via high-speed FACS analysis. Alternatively, B6.SJL whole bone marrow cells were injected in lethally irradiated BALB/ c mice (10 Gy). One, 3, 6, and 24 h after transplant, marrow was harvested and cells were either plated for high proliferative potential colony-forming cell (HPP-CFC) assay or secondarily injected into myeloablated (8 Gy) C57BL/6J mice using 10% competing C57BL/6J marrow. Chimerism was evaluated at 8 weeks. CFSE+ cells were detected in the bone marrow 1, 3, and 6 h after injection. The numbers were moderately lower when compared to syngeneic homing possibly due to strain effect. Conversely, utilizing a surrogate or secondary assay, we observed a decline of secondary engraftment of harvested cells over time, but not of HPP-CFC. Combining experiments and normalizing the 1-h time point to 100% (to allow comparison), we observed a mean relative engraftment of 87 ± 29%, 72 ± 21%, 84 ± 35% of the 1 h level at 3, 6, and 24 h respectively. HPP-CFC assay showed no significant variation as a homing surrogate over 1-6 h. These data indicate a rapid homing into allogeneic recipients with a plateau at 1 h. The decline of secondary engraftability over time may indicate a phenotype alteration of homed cells.Hematopoetic stem cells (HSC) are defined by their capacity to fully reconstitute marrow of lethally irradiated hosts and give rise to all marrow-derived hematopoietic elements. Stem cell transplantation is a clinical approach used to restore defective hematopoiesis due either to highdose chemoradiotherapy or to intrinsic marrow diseases. In this process, intravenously infused stem cells rapidly find their way to specific periendosteal location in the marrow-termed niches. The totality of this process defines homing . Using syngeneic inbred mice, many aspects of stem cell homing have been described (Vos et al

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“…This is followed by the activation of chemokine receptors and integrins that results in high affinity binding to immunoglobulin superfamily ligands, and enables firm adhesion and transmigration through the endothelial barrier [2,3]. Thus far, studies investigating the molecular interactions that regulate the trafficking of HSCs have established the importance of the chemokine receptor CXCR4/CXCL12 ligand [4][5][6][7] and a4b1 integrin/vascular cell adhesion molecule-1 (VCAM-1) adhesion pathways [8][9][10][11][12] for HSCs to home to the BM microenvironment of irradiated recipients. However, despite the identification of a few molecules that have been linked to the HSC homing process, the molecular mechanisms underlying the homing of transplanted HSCs to the BM remain largely unknown.…”

Section: Introductionmentioning

confidence: 99%

“…The a4 (CD49d) subunit can pair with b1 (CD29) (a4b1 integrin; also known as very late antigen-4 [VLA-4]) to bind VCAM-1 or b7 (a4b7 integrin; also known as lymphocyte Peyer's patch adhesion molecule-1 [LPAM-1]) to bind mucosal addressin cell adhesion molecule-1 (MAdCAM-1) [13]. The a4b1 integrin/VCAM-1 interaction plays an important role in HSC homing to the BM [8][9][10][11][12], but further studies are required to dissect the exact role of a4b7 integrin in HSC trafficking.…”

Section: Introductionmentioning

confidence: 99%

Evidence that β7 Integrin Regulates Hematopoietic Stem Cell Homing and Engraftment Through Interaction with MAdCAM-1

Murakami

Franco

et al. 2016

Stem Cells and Development

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a4b7 integrin is a cell adhesion receptor that is crucial for the migration of hematopoietic progenitors and mature effector cells in the periphery, but its role in adult hematopoiesis is controversial. We identified a subset of hematopoietic stem cells (HSCs) in the bone marrow (BM) that expressed b7 integrin. These b7 + HSCs were capable of multilineage, long-term reconstitution and had an inherent competitive advantage over b7 -HSCs. On the other hand, HSCs that lacked b7 integrin (b7KO) had reduced engraftment potential. Interestingly, quantitative RT-PCR and flow cytometry revealed that b7KO HSCs expressed lower levels of the chemokine receptor CXCR4. Accordingly, b7KO HSCs exhibited impaired migration abilities in vitro and BM homing capabilities in vivo. Lethal irradiation induced expression of the a4b7 integrin ligand-mucosal addressin cell adhesion molecule-1 (MAdCAM-1) on BM endothelial cells. Moreover, blocking MAdCAM-1 reduced the homing of HSCs and impaired the survival of recipient mice. Altogether, these data indicate that b7 integrin, when expressed by HSCs, interacted with its endothelial ligand MAdCAM-1 in the BM microenvironment, thereby promoting HSC homing and engraftment.

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Endothelial selectins and vascular cell adhesion molecule-1 promote hematopoietic progenitor homing to bone marrow

Cited by 355 publications

References 35 publications

Endothelial NOS is required for SDF-1α/CXCR4-mediated peripheral endothelial adhesion of c-kit+ bone marrow stem cells

Endothelial NOS is required for SDF-1α/CXCR4-mediated peripheral endothelial adhesion of c-kit+ bone marrow stem cells

Murine allogeneic in vivo stem cell homing^,

Evidence that β7 Integrin Regulates Hematopoietic Stem Cell Homing and Engraftment Through Interaction with MAdCAM-1

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Endothelial selectins and vascular cell adhesion molecule-1 promote hematopoietic progenitor homing to bone marrow

Cited by 355 publications

References 35 publications

Endothelial NOS is required for SDF-1α/CXCR4-mediated peripheral endothelial adhesion of c-kit+ bone marrow stem cells

Endothelial NOS is required for SDF-1α/CXCR4-mediated peripheral endothelial adhesion of c-kit+ bone marrow stem cells

Murine allogeneic in vivo stem cell homing,

Evidence that β7 Integrin Regulates Hematopoietic Stem Cell Homing and Engraftment Through Interaction with MAdCAM-1

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Product

Resources

About

Murine allogeneic in vivo stem cell homing^,