Cytokines active on granulomonopoiesis: release and consumption by human marrow myeloid stromal cells

Sensebé, Luc; Mortensen, Børge Thing; Fixe, P.; Hervé, P.; Charbord, Pierre

doi:10.1046/j.1365-2141.1997.1953012.x

Cited by 15 publications

(8 citation statements)

References 42 publications

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“…Under normoxic control conditions of the present study, hBMSCs synthesized VEGF and TGFβ1 at the mRNA and protein levels. These findings are in agreement with literature reports that human and murine BMSCs used for cell therapy or feeder layer purposes expressed VEGF (Kinnaird et al, 2004b) and TGFβ1 (Han et al, 2005;Sensebe et al, 1997). Under our control conditions, however, almost no bFGF expression was detected at the protein level, contrary to previous studies (Han et al, 2005;Kinnaird et al, 2004b), probably due to differences in the experimental conditions, such as the cell density used.…”

Section: Discussionsupporting

confidence: 92%

Desferrioxamine‐driven upregulation of angiogenic factor expression by human bone marrow stromal cells

Potier¹,

Ferreira²,

Dennler³

et al. 2008

J Tissue Eng Regen Med

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Bone marrow stromal cells (BMSCs) are the subject of intense research because of their biological properties and potential use for the repair of damaged tissues. Success of BMSC-based therapies, however, relies on a number of methodological improvements, including the establishment of a vascular network providing nutrients and oxygen to the transplanted cells and ensuring their immediate survival and long-term functionality. We described a method to enhance the autocrine expression of angiogenic factors by BMSCs. For this purpose, human BMSCs were treated with desferrioxamine (DFX). No PDGF-BB, VEGF-R1 or -R2 mRNA expression was detected under any of the conditions tested. mRNA and protein expression levels of TGFbeta1 were similar in BMSCs, whether they were exposed to DFX (50 microM) or to control conditions under normoxia for 48 h. In comparison with the results obtained with control conditions under normoxia, exposure of BMSCs to DFX for 48 h resulted in upregulation of bFGF at the protein (26-fold) but not at the mRNA levels and VEGF at both the mRNA (1.5-fold) and protein levels (4.5-fold). In comparison with the results obtained with control conditions under hypoxia, DFX induced a 50% increase in VEGF secretion but led to the same level of hypoxia inducible factor-1alpha protein expression (a transduction factor involved in angiogenic factor expression and known to be activated by DFX). Exposure of BMSCs to DFX resulted in oversecretion of angiogenic factors, suggesting that DFX-treated BMSCs could be used to supply angiogenic factors.

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Section: Discussionsupporting

confidence: 92%

Desferrioxamine‐driven upregulation of angiogenic factor expression by human bone marrow stromal cells

Potier¹,

Ferreira²,

Dennler³

et al. 2008

J Tissue Eng Regen Med

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“…15,16 Marrow stromal layers express a multitude of factors that may be important in the positive and negative regulation of hematopoiesis. 16,28,29 Downregulation or upregulation of the expression or production of some of those factors has been implicated as a possible cause for the reduced capacity of stromal layers to support in vitro hematopoiesis that is observed with some malignancies, viral infections and poor marrow recovery after marrow transplantation. 19,[30][31][32][33][34]44 Previous studies implicated TNF-␣, IL-4 and IFN-␣ as factors partially responsible for the reduced capacity of HIVinfected stromal layers to support the proliferation of normal donor CD34 + cells.…”

Section: Discussionmentioning

confidence: 99%

“…7,19,21,23,24,26,27 A variety of stimulatory and negative factors that regulate the proliferation and differentiation of hematopoietic progenitors are expressed in the marrow microenvironment. 6,[28][29][30] Two of the possible causes for hematopoietic deficiencies observed after chemotherapy are either a decrease in production of stimulatory factors or an increase in the production Table 1 Recovery of committed and primitive progenitors in post-chemotherapy marrow CD34 + cells …”

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confidence: 99%

Post-chemotherapy and cytokine pretreated marrow stromal cell layers suppress hematopoiesis from normal donor CD34+ cells

Schwartz

Warren

Rothwell

et al. 1998

Bone Marrow Transplant

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Summary:Marrow stromal layers were used to investigate the potential role of negative regulators produced by the marrow microenvironment as one potential cause of hematopoietic suppression after chemotherapy and cytokines. Stromal layers were established from marrow of normal or prechemotherapy donors and breast cancer patients after hematological recovery from one cycle of 5-fluorouracil, leucovorin, doxorubicin, and cyclophosphamide and GM-CSF or PIXY321 (GM-CSF/IL-3 fusion protein). Normal donor CD34 + cells were placed in contact with stromal layers, and the number of colony-forming units for granulocytes and macrophages (CFU-GM) was determined. There were 25-79% fewer CFU-GM in post-chemotherapy stromal layer cocultures than in no chemotherapy cocultures. With neutralizing antibody to TNF-␣ the number of CFU-GM in no chemotherapy and post-chemotherapy stromal cocultures was, respectively, 96 ؎ 7% (n = 5) and 142 ؎ 8% (n = 5) of the number with no antibody treatment. PIXY321 and GM-CSF pretreated stromal layers also suppressed production of CFU-GM. Anti-TNF-␣ promoted an increase in CFU-GM numbers from GM-CSF, but not PIXY321, pretreated stromal cocultures. The results demonstrate that post-chemotherapy marrow stromal layers were deficient in supporting in vitro hematopoiesis and suggest that negative regulators induced by chemotherapy and cytokines may be one cause for this defect.

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“…G-CSF (100 ng/ml) and EPO (10 U/ml) induced a 100% increase in the number of tubes (versus a maximum increase of 78% using 0.1 ng/ml of VEGF, the optimal concentration for capillary tube increase). Marrow stromal cells are known to synthesize G-CSF, GM-CSF, EPO, and SCF (Bulabois et al, 1998;Sensebe, et al, 1997a;1997b). However, G-CSF synthesis is observed only after induction by inflammatory cytokines; EPO and SCF synthesis is variable from one layer to the other or when induced by IL-1; and GM-CSF release is minimal in the absence of IL-1.…”

Section: Role Of Hematopoietic Cytokinesmentioning

confidence: 99%

An In Vitro Model for the Study of Human Bone Marrow Angiogenesis: Role of Hematopoietic Cytokines

Pelletier¹,

Regnard²,

Fellmann³

et al. 2000

Laboratory Investigation

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SUMMARY:This study describes a human bone marrow endothelial cell culture in which endothelial cells are organized into capillary tubes. These endothelial cells were positive for von Willebrand Factor, expressed CD34, CD31, and L-fucose residues, took up acetylated low-density lipoproteins, contained Weibel-Palade bodies, and were ensheathed in a basal lamina (which included laminin ␤1, EDaϩ and EDbϩ fibronectin, and collagen type iv). Pericytes expressing ␣-smooth muscle (␣-SM) actin were spatially associated with the capillary tubes and there was a highly significant correlation between the number of capillary tubes and pericytes. In this model, basal angiogenesis was found to be vascular endothelial growth factor (VEGF)-dependent, because neutralization of endogenous VEGF induced a dramatic regression in the number of tubes. However, the presence of ␣-SM actin-expressing pericytes in the linings of endothelial tubes partially prevented the VEGF-neutralized tube regression. We also observed that nitric oxide production contributed to basal angiogenesis and that upregulation of nitric oxide increased the number of tubes. Tube numbers also decreased when antibodies neutralizing the integrin ␣v␤5 were applied to the cultures. Moreover, addition of any of the hematopoietic cytokines, erythropoietin, stem cell factor, granulocytic colony stimulating factor, or granulomonocytic colony stimulating factor induced a highly significant increase in tube formation. When erythropoietin and granulocytic colony stimulating factor were added, this increase was larger than the maximum increase observed with VEGF. Thus, we have described an in vitro model for human bone marrow angiogenesis in which pericytes and basal lamina matrix were associated with endothelial cells and formed fully organized capillary tubes. In this model, cytokines known to regulate hematopoiesis also seemed to be mediators of angiogenesis. This culture system may therefore prove to be a valuable tool for the study of hematopoietic cytokines on angiogenesis. (Lab Invest 2000, 80:501-511).

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Cytokines active on granulomonopoiesis: release and consumption by human marrow myeloid stromal cells

Cited by 15 publications

References 42 publications

Desferrioxamine‐driven upregulation of angiogenic factor expression by human bone marrow stromal cells

Desferrioxamine‐driven upregulation of angiogenic factor expression by human bone marrow stromal cells

Post-chemotherapy and cytokine pretreated marrow stromal cell layers suppress hematopoiesis from normal donor CD34+ cells

An In Vitro Model for the Study of Human Bone Marrow Angiogenesis: Role of Hematopoietic Cytokines

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