Hematopoietic Progenitor Cell Rolling in Bone Marrow Microvessels: Parallel Contributions by Endothelial Selectins and Vascular Cell Adhesion Molecule 1

Mazo, Irina B.; Gutierrez‐Ramos, José Carlos; Frenette, Paul S.; Hynes, Richard O.; Wagner, Denisa D.; Andrian, Ulrich H. von

doi:10.1084/jem.188.3.465

Cited by 402 publications

(392 citation statements)

References 46 publications

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“…33,34 Indeed CD49d/VCAM-1 interactions have been shown to play an important role in the homing of progenitor cells back to the bone marrow. 35,36 It has previously been shown that CD49d expressed on neutrophils mediates interactions with VCAM-1 29 ; therefore, it is likely that neutrophil release is VCAM-1 dependent. However, there is also a precedent in the literature, in a model of chronic vasculitis, for CD49d/CD29-mediated neutrophil adhesion to be independent of VCAM-1.…”

Section: Discussionmentioning

confidence: 99%

The CXC chemokine MIP-2 stimulates neutrophil mobilization from the rat bone marrow in a CD49d-dependent manner

Burdon

Martin

Rankin

2005

Blood

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The acute release of neutrophils from the bone marrow is a critical step in their trafficking to sites of inflammation. This process is stimulated by systemically acting inflammatory mediators, such as the CXC chemokines. In this study we have used a novel in situ perfusion system of the rat femoral bone marrow to directly investigate the role of specific adhesion molecules in chemokine-stimulated neutrophil mobilization. We show here that neutrophils mobilized in response to rat macrophage inflammatory protein-2 (MIP-2) shed L-selectin and expressed significantly higher levels of CD11b and CD49d. However, inhibition of L-selectin sheddase activity with KD-IX-73-4 had no effect on the number of neutrophils mobilized in response to rat MIP-2. Blockade of CD18, using a neutralizing monoclonal antibody (mAb), did not inhibit neutrophil mobilization but unexpectedly increased the rate and number of neutrophils released from the bone marrow in response to chemokine, suggesting that CD18 could play a role in neutrophil retention within the bone marrow. Blockade of CD49d using either a selective mAb or a specific antagonist resulted in a dramatic inhibition (> 75%) of the chemokine-stimulated neutrophil mobilization from the bone marrow. These data reveal contrasting roles for CD18 and CD49d in the retention and release of neutrophils from the bone marrow. (Blood. 2005;105:2543-2548)

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Section: Discussionmentioning

confidence: 99%

The CXC chemokine MIP-2 stimulates neutrophil mobilization from the rat bone marrow in a CD49d-dependent manner

Burdon

Martin

Rankin

2005

Blood

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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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“…48 The use of fluorescent probe intravenous injection combined with intravital microscopy of mouse calvaria was introduced by Von Andrian's team. 49 Twophoton fluorescence can be collected through the bone cortex via a confocal microscope as long as that the cortex is flat and thin enough, which makes mouse calvaria the best candidate for this imaging technique. After mouse anesthesia, fluorescent tracers (Rhodamine/fluorescein isothiocyanate-labeled dextran or smaller particles such as quantum dots) are injected into the blood circulation followed by observation under the confocal microscope.…”

Section: Vessel Wall Labelingmentioning

confidence: 99%

Assessment of bone vascularization and its role in bone remodeling

Lafage-Proust¹,

Roche²,

Langer³

et al. 2015

BoneKEy Reports

108

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Bone is a composite organ that fulfils several interconnected functions, which may conflict with each other in pathological conditions. Bone vascularization is at the interface between these functions. The roles of bone vascularization are better documented in bone development, growth and modeling than in bone remodeling. However, every bone remodeling unit is associated with a capillary in both cortical and trabecular envelopes. Here we summarize the most recent data on vessel involvement in bone remodeling, and we present the characteristics of bone vascularization. Finally, we describe the various techniques used for bone vessel imaging and quantitative assessment, including histology, immunohistochemistry, microtomography and intravital microscopy. Studying the role of vascularization in adult bone should provide benefits for the understanding and treatment of metabolic bone diseases.

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Hematopoietic Progenitor Cell Rolling in Bone Marrow Microvessels: Parallel Contributions by Endothelial Selectins and Vascular Cell Adhesion Molecule 1

Cited by 402 publications

References 46 publications

The CXC chemokine MIP-2 stimulates neutrophil mobilization from the rat bone marrow in a CD49d-dependent manner

The CXC chemokine MIP-2 stimulates neutrophil mobilization from the rat bone marrow in a CD49d-dependent manner

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

Assessment of bone vascularization and its role in bone remodeling

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