Increased binding and defective migration across fibronectin of cycling hematopoietic progenitor cells

Giet, Olivier; Bockstaele, Dirk R. Van; Stefano, Ivano Di; Huygen, Sandra; Greimers, Roland; Béguin, Yves; Gothot, André

doi:10.1182/blood.v99.6.2023

Cited by 23 publications

(21 citation statements)

References 43 publications

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“…In contrast, cells in G0 are more frequently not adhered. This suggests that cell cycle transition is associated with adhesion to fibronectin (33,34). However, the activation of the cell cycle does not cause adhesion of the cell to fibronectin since cells in various stages of the cell cycle have been found in non-adherent fractions.…”

Section: Discussionmentioning

confidence: 94%

Protein-energy malnutrition halts hemopoietic progenitor cells in the G0/G1 cell cycle stage, thereby altering cell production rates

Borelli

Barros

Nakajima

et al. 2009

Braz J Med Biol Res

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Protein energy malnutrition (PEM) is a syndrome that often results in immunodeficiency coupled with pancytopenia. Hemopoietic tissue requires a high nutrient supply and the proliferation, differentiation and maturation of cells occur in a constant and balanced manner, sensitive to the demands of specific cell lineages and dependent on the stem cell population. In the present study, we evaluated the effect of PEM on some aspects of hemopoiesis, analyzing the cell cycle of bone marrow cells and the percentage of progenitor cells in the bone marrow. Two-month-old male Swiss mice (N = 7-9 per group) were submitted to PEM with a low-protein diet (4%) or were fed a control diet (20% protein) ad libitum. When the experimental group had lost about 20% of their original body weight after 14 days, we collected blood and bone marrow cells to determine the percentage of progenitor cells and the number of cells in each phase of the cell cycle. Animals of both groups were stimulated with 5-fluorouracil. Blood analysis, bone marrow cell composition and cell cycle evaluation was performed after 10 days. Malnourished animals presented anemia, reticulocytopenia and leukopenia. Their bone marrow was hypocellular and depleted of progenitor cells. Malnourished animals also presented more cells than normal in phases G0 and G1 of the cell cycle. Thus, we conclude that PEM leads to the depletion of progenitor hemopoietic populations and changes in cellular development. We suggest that these changes are some of the primary causes of pancytopenia in cases of PEM.

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Section: Discussionmentioning

confidence: 94%

Protein-energy malnutrition halts hemopoietic progenitor cells in the G0/G1 cell cycle stage, thereby altering cell production rates

Borelli

Barros

Nakajima

et al. 2009

Braz J Med Biol Res

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“…37,38 At the stage of enucleating erythroblast/reticulocyte the ␤1 integrins are lost from the cell surface and circulating RBCs do not express these receptors. 39 In addition, ␤1 integrins, especially ␣4␤1 and ␣5␤1, are expressed on human CD34 ϩ hematopoietic stem and progenitor and long-term culture-initiating cells (LTC-ICs) and are involved in fibronectin binding and transendothelial migration 40 as well as engraftment of human hematopoieticrepopulating cells in nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice. 41 Our data demonstrate that parvovirus B19 internalization into purified human erythroid progenitor cells can be completely inhibited by antibodies blocking ␤1 integrin function, corroborating the notion that ␤1 integrins play a crucial role in parvovirus B19 infection of its natural target cells.…”

Section: Discussionmentioning

confidence: 99%

α5β1 integrin as a cellular coreceptor for human parvovirus B19: requirement of functional activation of β1 integrin for viral entry

Weigel-Kelley

Yöder

Srivastava

2003

Blood

216

156

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Replication of the pathogenic human parvovirus B19 is restricted to erythroid progenitor cells. Although blood group P antigen has been reported to be the cell surface receptor for parvovirus B19, a number of nonerythroid cells, which express P antigen, are not permissive for parvovirus B19 infection. We have documented that P antigen is necessary for parvovirus B19 binding but not sufficient for virus entry into cells. To test whether parvovirus B19 utilizes a cell surface coreceptor for entry, we used human erythroleukemia cells (K562), which allow parvovirus B19 binding but not entry. We report here that upon treatment with phorbol esters, K562 cells become adherent and permissive for parvovirus B19 entry, which is mediated by ␣5␤1 integrins, but only in their high-affinity conformation. Mature human red blood cells (RBCs), which express high levels of P antigen, but not ␣5␤1 integrins, bind parvovirus B19 but do not allow viral entry. In contrast, primary human erythroid progenitor cells express high levels of both P antigen and ␣5␤1 integrins and allow ␤1 integrin-mediated entry of parvovirus B19. Thus IntroductionTwo parvoviruses of human origin, the nonpathogenic adenoassociated virus 2 (AAV) and the pathogenic parvovirus B19, have been studied extensively. 1,2 Recombinant AAV vectors have gained attention as a potentially useful alternative to the more commonly used recombinant retroviral and adenoviral vectors in human gene therapy. 3 AAV possesses a broad host range that transcends the species barrier because it utilizes the ubiquitously expressed cell surface heparan sulfate proteoglycan as a primary receptor for viral binding. 4 We and others have reported the requirement of fibroblast growth factor receptor 1 (FGFR1) and ␣V␤5 integrin as coreceptors for viral entry. 5,6 Parvovirus B19, on the other hand, has been shown to have an extremely limited tissue-tropism, and the virus replication is restricted to human erythroid progenitor cells, 7 presumably because (1) the blood group P antigen (synonym "globoside"; "globotetraosylceramide") is used as primary cellular receptor for parvovirus B19, 8 (2) putative intracellular factors, largely restricted to human erythroid cells, are required for optimal transcriptional activation of the B19 promoter at map unit 6 (B19p6) and viral replication, 9,10 and (3) B19 capsid protein expression in nonpermissive cells is impaired due to a block in full-length transcription of the viral genome, atypical mRNA splicing, and impaired ribosome loading of structural gene transcripts. [11][12][13] However, P antigen expression is not restricted to erythroid cells, and a number of P antigen-positive nonerythroid cells are nonpermissive for a successful infection by parvovirus B19. 2 In addition, mature red blood cells (RBCs), which are known to express high levels of P antigen, are unlikely to be ideal targets for B19 infection and replication because they lack nuclei. Similarly, B19p6 promoter-driven expression analyses were carried out with plasmid DNA transfections, 11...

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“…5 Homing begins with the chemoattraction of CD133 ϩ cells to the bone marrow and progresses to their extravasation across bone marrow sinusoidal endothelium and their transmigration through the basal lamina to specific hematopoietic stem cell/hematopoietic progenitor cell (HSC/HPC) niches. [5][6][7][8][9][10][11][12][13][14][15][16] The chemokine CXCL12 plays a central role as a chemoattractant for CD133 ϩ HSCs/HPCs, regulating their motility, homing to, and retention, survival, and proliferation in the bone marrow (for reviews, see Burger and Kipps, 12 Broxmeyer et al, 17 Kollet et al, 18 and Kim et al 19 ). CXCL12 is the ligand for CXCR4, a 7-transmembrane G-protein-coupled receptor (for reviews, see Burger and Kipps 12 and Zou et al 14 ).…”

Section: Introductionmentioning

confidence: 99%

Endolyn (CD164) modulates the CXCL12-mediated migration of umbilical cord blood CD133+ cells

Forde

Tye

Newey

et al. 2006

Blood

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Hematopoietic stem cell/hematopoietic progenitor cell (HSC/HPC) homing to specific microenvironmental niches involves interactions between multiple receptor ligand pairs. Although CXCL12/CXCR4 plays a central role in these events, CXCR4 regulators that provide the specificity for such cells to lodge and be retained in particular niches are poorly defined. Here, we provide evidence that the sialomucin endolyn (CD164), an adhesion receptor that regulates the adhesion of CD34 ؉ cells to bone marrow stroma and the recruitment of CD34 ؉ CD38 lo/؊ cells into cycle, associates with CXCR4. The class II 103B2 monoclonal antibody, which binds the CD164 N-linked glycan-dependent epitope or CD164 knockdown by RNA interference, significantly inhibits the migration of CD133 ؉ HPCs toward CXCL12 in vitro. On presentation of CXCL12 on fibronectin, CD164 associates with CXCR4, an interaction that temporally follows the association of CXCR4 with the integrins VLA-4 and VLA-5. This coincides with PKC-and Akt signaling through the CXCR4 receptor, which was disrupted on the loss of CD164 though MAPK signaling was unaffected. We therefore demonstrate a novel association among 3 distinct families of cell-surface receptors that regulate cell migratory responses and identify a new role for CD164. We propose that this lends specificity to the homing and lodgment of these cells within the bone marrow niche. IntroductionAn important determinant of successful stem cell transplantation is the ability of transplanted cells to mobilize, home, migrate, and efficiently engraft and repair damaged tissues with functional cells. It is now standard practice to mobilize CD133 ϩ CD34 ϩ cells from bone marrow into the circulation by administering G-CSF or to collect such cells from umbilical cord blood and to use these for transplantation. [1][2][3][4] Once administered, these cells home to the bone marrow, where they engraft in specific stromal or vascular niches. 5 Homing begins with the chemoattraction of CD133 ϩ cells to the bone marrow and progresses to their extravasation across bone marrow sinusoidal endothelium and their transmigration through the basal lamina to specific hematopoietic stem cell/hematopoietic progenitor cell (HSC/HPC) niches. [5][6][7][8][9][10][11][12][13][14][15][16] The chemokine CXCL12 plays a central role as a chemoattractant for CD133 ϩ HSCs/HPCs, regulating their motility, homing to, and retention, survival, and proliferation in the bone marrow (for reviews, see Burger and Kipps,12 Broxmeyer et al, 17 Kollet et al, 18 and Kim et al 19 ). CXCL12 is the ligand for CXCR4, a 7-transmembrane G-protein-coupled receptor (for reviews, see Burger and Kipps 12 and Zou et al 14 ). Although lethal in the perinatal period, identical and significant reductions in B-lymphopoiesis and myelopoiesis have been described during fetal development in mice deficient in CXCL12 and CXCR4. 20,21 B-lymphopoiesis and myelopoiesis are both regulated by the interactions of their precursors, with specific microenvironmental niches within the bone mar...

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Increased binding and defective migration across fibronectin of cycling hematopoietic progenitor cells

Cited by 23 publications

References 43 publications

Protein-energy malnutrition halts hemopoietic progenitor cells in the G0/G1 cell cycle stage, thereby altering cell production rates

Protein-energy malnutrition halts hemopoietic progenitor cells in the G0/G1 cell cycle stage, thereby altering cell production rates

α5β1 integrin as a cellular coreceptor for human parvovirus B19: requirement of functional activation of β1 integrin for viral entry

Endolyn (CD164) modulates the CXCL12-mediated migration of umbilical cord blood CD133+ cells

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