Proteoglycans on bone marrow endothelial cells bind and present SDF-1 towards hematopoietic progenitor cells

Netelenbos, Tanja; Born, J van den; Kessler, Floortje L.; Zweegman, Sonja; Merle, Pauline A.; Oostveen, J. W. Van; Zwaginga, Jaap Jan; Huijgens, Peter C.; Dräger, A.M.

doi:10.1038/sj.leu.2402738

Cited by 84 publications

(74 citation statements)

References 57 publications

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“…37 Chondroitin sulfate has been shown to be required for cellular binding of SDF-1. 38 In prostate carcinoma, treatment of cancer cells with SDF-1 upregulated expression of a v b 3 integrin receptors, resulting in increased cell adhesion and invasion. 39 Furthermore, SDF-1 has been shown to be critical for spread of prostate cancer, and a positive correlation has been reported between SDF-1 signaling and bony metastasis.…”

Section: Discussionmentioning

confidence: 99%

Increased expression of non-sulfated chondroitin correlates with adverse clinicopathological parameters in prostate cancer

et al. 2008

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Chondroitin sulfate is a structurally diverse glycosaminoglycan, which contains a variable degree of sulfation that helps to determine its biological function. It is involved in the regulation of cellular activity and has been implicated in carcinogenesis. To determine if the non-sulfated chondroitin backbone has a functional role in prostate cancer, we analyzed its expression by immunohistochemistry using the 1B5 monoclonal antibody and a set of tissue microarrays constructed with 227 prostate specimen cores from 81 cases of benign prostate tissue and 77 cases of prostate cancer, of which 69 of these cases are matched. Non-sulfated chondroitin was found in the secretory epithelial cells and stromal regions of both prostatic adenocarcinoma and benign prostatic tissues, as well as in the basal cells of benign glands. A higher percentage of cancerous cells were stained positively for non-sulfated chondroitin as compared with benign secretory cells of the same patient. Cancerous cells stained more intensely for non-sulfated chondroitin. This increase in percentage of cells stained and increase in staining intensity were associated with higher pathological T stage and extraprostatic extension. Non-sulfated chondroitin expression (either staining intensity or percentage of cells stained) in adenocarcinoma and its peritumoral stroma correlated significantly with several clinicopathological parameters of unfavorable outcome, including higher pathological T stage and Gleason score, presence of tumor in both prostatic lobes, extraprostatic extension, seminal vesicle involvement and preoperative prostate-specific antigen levels. These data suggest that non-sulfated chondroitin is a potentially useful biomarker for prostate cancer, and may be involved in regulating prostate cancer behavior.

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Section: Discussionmentioning

confidence: 99%

Increased expression of non-sulfated chondroitin correlates with adverse clinicopathological parameters in prostate cancer

et al. 2008

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“…Presence of HUVEC on the transwell filter, with their own ECM and its ability to bind and present SDF1 [16] and the ability to process and re-secrete functional SDF1 [33] was found to further enhance the migratory response of HSPC in the investigated systems. This could explain the effect that we observe for sample SDF1 (1)-H on Fig2, 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 Hematopietic progenitor cells migrate selectively to the SDF-1 gradient [34].…”

Section: Discussionmentioning

confidence: 95%

“…Sulphated GAGs, in particular heparan sulphate, exhibit a particularly high affinity to SDF1 and have been reported to support presentation of SDF1 to the vascular lumen in the stem cell niche [16][17]30].…”

Section: Discussionmentioning

confidence: 99%

“…Several earlier studies described the adsorption of SDF1 to tissue culture plastic [15], heparin coated dishes [16][17], or fibronectin layers [18] with the aim to manipulate the migratory response of HSPC and/or the adhesion of T cells to immobilized SDF1. All of those studies used two-dimensional culture systems with limited SDF1 loading capacity that is not amenable for in vivo studies.…”

Section: Introductionmentioning

confidence: 99%

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Prolonged transendothelial migration of human haematopoietic stem and progenitor cells (HSPCs) towards hydrogel-released SDF1

et al. 2011

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The therapeutic success of haematopoetic stem and progenitor cell (HSPC) transplantation is critically dependent on HSPC engraftment in the bone marrow. Gradients of stromal cell derived factor 1 (SDF1) direct HSPC homing both in vitro and vivo. Potentially, regulating delivery levels of exogenous SDF1 applied to the bone marrow could augment HSPC engraftment. Thus the aim of the present study was to revise the ability of biocompatible hydrogels to direct HSPC migration in vitro.The delivery system of choice is based on heparin cross-linked with Collagen1. We confirm that hydrogel is capable to trap and release SDF1 and used it to generate protein gradient in transendothelial (Human Umbilical Vein Endothelial Cell -HUVEC) migration experiments. The use of SDF1 functionalised hydrogel to produce chemokine gradient revealed sustained and increased HSPC migration when compared to diffusible SDF1 controls.In conclusion, regulating SDF1 gradients with heparin-containing hydrogels may offer valuable options to direct site-specific migration of HSPC.

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“…Transendothelial Cell Migration Assay-Transendothelial cell migration was performed using trans-wells containing 3-m pore-polycarbonate filters to separate the upper and lower chambers in 24-well plates (Costar, Cambridge, MA) (20,21). Immortalized mouse lung endothelial cells (22,23) were seeded at 1.5 ϫ 10 4 per well in the upper chamber and became confluent after 3-4 days in culture.…”

Section: Methodsmentioning

confidence: 99%

Heparin-induced Leukocytosis Requires 6-O-Sulfation and Is Caused by Blockade of Selectin- and CXCL12 Protein-mediated Leukocyte Trafficking in Mice

Zhang

Condac

Qiu

et al. 2012

Journal of Biological Chemistry

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Background: Heparin-induced leukocytosis (HIL) is commonly seen in patients. Results: In mice, heparin requires 6-O-sulfation to induce leukocytosis. Heparin alters selectin-and/or CXCL12-mediated lymphocyte homing and release, neutrophil release, and distribution in the vasculature. Conclusion: HIL requires 6-O-sulfation and is caused by blocking selectin-and CXCL12-mediated leukocyte trafficking. Significance: This study elucidated the structural determinants and the underlying mechanisms of heparin in HIL.

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Proteoglycans on bone marrow endothelial cells bind and present SDF-1 towards hematopoietic progenitor cells

Cited by 84 publications

References 57 publications

Increased expression of non-sulfated chondroitin correlates with adverse clinicopathological parameters in prostate cancer

Increased expression of non-sulfated chondroitin correlates with adverse clinicopathological parameters in prostate cancer

Prolonged transendothelial migration of human haematopoietic stem and progenitor cells (HSPCs) towards hydrogel-released SDF1

Heparin-induced Leukocytosis Requires 6-O-Sulfation and Is Caused by Blockade of Selectin- and CXCL12 Protein-mediated Leukocyte Trafficking in Mice

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