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At least 19 recordsLinked to original sources
PubMed2004

Prostate cancer cell adhesion to bone marrow endothelium: the role of prostate-specific antigen.

Bone metastasis is the most frequent complication of prostate cancer (PC). Elucidation of the biological basis of this specificity is required for the development of approaches for metastatic inhibition. We investigated the possibility that the preferential attachment of PC cells to bone marrow endothelium (as opposed to endothelium from other organs) affects this specificity. We selected, from peptide phage-displayed libraries, peptide ligands to surfaces of PC cells (C4-2B) attenuated (30-40%) binding of C4-2B cells to bone marrow endothelial cells (BMECs). We then determined the molecules on the surface of C4-2B cells interacted with the selected peptides using column affinity chromatography and a cDNA expression phage-displayed library generated from C4-2B cells in T7 phage. We identified a phage from the cDNA library that specifically bound to one of the selected peptides-L11. This phage displayed the amino acid sequence homologous for the COOH-terminal portion of prostate-specific antigen (PSA). To examine the possible direct involvement of PSA in the interactions between PC and BMECs, we performed a cell-cell adhesion assay. Antibodies to PSA attenuated PC cells adhesion to BMECs. In addition, exogenous proteolytically active PSA modulated this adhesion. Finally, inactivation of mRNA coding PSA by a small interfering RNA (siRNA) diminished C4-2B cell adhesion to BMECs. These results indicate that PSA expressed as secreted and surface-associated molecules in C4-2B cells is involved in cell-cell interactions and/or digests components of bone marrow endothelium for preferential adhesion and penetration of PC cells. The suggested experimental approach is a promising strategy for identification of cell surface molecules involved in intercellular interactions.

Apoptosis↗
PubMed2001

Interactions of human prostatic epithelial cells with bone marrow endothelium: binding and invasion.

Prostate cancer shows a propensity to form secondary tumours within the bone marrow. Such tumours are the major cause of mortality in this disease. We have developed an in vitro system to study the binding of prostate epithelial cells to bone marrow endothelium (BME) and stroma (BMS). The metastatic prostate cancer cell line, PC3 (derived from a bone metastasis), was seeded onto confluent layers of BME and its binding characteristics compared to human umbilical vein endothelial cells (HUVEC), lung endothelium (Hs888Lu) and BMS. The PC3 cell line showed significantly increased binding to BME (P< 0.05) compared to endothelium derived from HUVEC and lung or BMS with maximal binding occurring at 1 h. Following pre-incubation with a beta1 integrin antibody PC3 binding to BME was inhibited by 64% (P< 0.001). Antibodies directed against the integrins beta4, alpha2, alpha4, alpha5 and the cellular adhesion molecules P-selectin, CD31, VCAM-1 and sialy Lewis X showed no effect on blocking PC3 binding. Primary prostatic epithelial cells from both malignant (n = 11) and non-malignant tissue (n = 11) also demonstrated equivalent levels of increased adhesion to BME and BMS compared to HUVEC, peaking at 24 h. Further studies examined the invasive ability of prostate epithelial cells in response to bone marrow endothelium using Matrigel invasion chamber assays. In contrast to the previous results, malignant cells showed an increase (1000 fold) in invasive ability, whilst non-malignant prostate epithelia did not respond. We have shown that both malignant and non-malignant prostate epithelial cells can bind at equivalent levels and preferentially to primary human bone marrow endothelium in comparison to controls. However, only malignant prostate epithelia show increased invasive ability in response to BME.

Adenocarcinoma↗
PubMed1986

Structural features of isolated, fractionated bone marrow endothelium compared to sinus endothelium in situ.

Structural features of isolated, fractionated rat bone marrow endothelium were compared to those of marrow sinus endothelium in situ. Marrow endothelium was purified, first by density gradient sedimentation on Percoll and then subjected to centrifugal elutriation. Using antifactor VIII antibody staining (indirect immunofluorescent method), preparations of greater than 50% purified endothelium were obtained. By SEM, these cells were about 10 microns in size and showed smooth surface and numerous invaginations. These features were also observed in the in situ endothelium obtained by perfusion-fixation and freeze-cracking. In addition, in situ endothelium displayed numerous hemopoietic cells in migration through the endothelium. By TEM, isolated endothelium showed numerous vesiculations, giving the cell sponge-like appearance. This corresponded to numerous intracellular vesicles in sinus endothelium in situ, reflecting high magnitude of fluid and molecular transport across the endothelium. Weibel-Palade bodies were not seen in either form of the endothelium, despite the positive reaction for factor VIII-related antigen. This finding suggested that the cell, while possessing factor VIII-related antigen, does not store this protein.

Animals↗
PubMed1994

Immuno-, lectin-, and enzyme-histochemical characterization of human bone marrow endothelium.

"Homing" of hematopoietic progenitor cells to the bone marrow occurs during the clinical practice of bone marrow transplantation. Its mechanism is unknown, although adhesive interactions between hematopoietic cells and sinusoidal endothelium in the bone marrow may be implicated. Studies of human bone marrow endothelial cells have previously been limited by the lack of markers for these cells. In this report, we describe positive staining of bone marrow endothelial cells from human bone marrow trephine biopsies with antibody to factor VIII-related antigen (FVIIIR-Ag) (Dako, High Wycombe, UK), the plant lectin Ulex europaeus agglutinin-I (UEA-I), and two mouse monoclonal antibodies, BMA120 and QBEND/10. In addition, alkaline phosphatase could be demonstrated in the majority of marrow endothelial cells using a novel enzyme histochemical technique. These studies defined the marker profile of human marrow endothelium. The results of this study will facilitate the isolation and culture of human marrow endothelial cells for in vitro studies of their roles in hematopoietic stem cell homing.

Alkaline Phosphatase↗
PubMed2002

Migration of human hematopoietic progenitor cells across bone marrow endothelium is regulated by vascular endothelial cadherin.

The success of stem cell transplantation depends on the ability of i.v. infused stem cells to engraft the bone marrow, a process referred to as homing. Efficient homing requires migration of CD34(+) cells across the bone marrow endothelium, most likely through the intercellular junctions. In this study, we show that loss of vascular endothelial (VE)-cadherin-mediated endothelial cell-cell adhesion increases the permeability of monolayers of human bone marrow endothelial cells (HBMECs) and stimulates the transendothelial migration of CD34(+) cells in response to stromal cell-derived factor-1alpha. Stromal cell-derived factor-1alpha-induced migration was dependent on VCAM-1 and ICAM-1, even in the absence of VE-cadherin function. Cross-linking of ICAM-1 to mimic the leukocyte-endothelium interaction induced actin stress fiber formation but did not induce loss of endothelial integrity, whereas cross-linking of VCAM-1 increased the HBMEC permeability and induced gaps in the monolayer. In addition, VCAM-1-mediated gap formation in HBMEC was accompanied by and dependent on the production of reactive oxygen species. These data suggest that modulation of VE-cadherin function directly affects the efficiency of transendothelial migration of CD34(+) cells and that activation of ICAM-1 and, in particular, VCAM-1 plays an important role in this process through reorganization of the endothelial actin cytoskeleton and by modulating the integrity of the bone marrow endothelium through the production of reactive oxygen species.

Antigens, CD↗
PubMed2002

Functional selectin ligands mediating human CD34(+) cell interactions with bone marrow endothelium are enhanced postnatally.

Hematopoietic progenitor cells (HPCs) can home to the bone marrow (BM) after a simple intravenous injection, but the adhesive mechanisms mediating the initial interactions of human HPCs with the BM endothelium have not been evaluated in vivo. Using fluorescence intravital microscopy and homing assays in NOD/SCID mice, we show that endothelial selectins are necessary for human adult CD34(+) cell homing, since rolling on BM endothelium and retention in the BM compartment are drastically reduced (>90%) in endothelial selectin-deficient NOD/SCID mice. Comparative analyses of CD34(+) cells collected from adults and from cord blood (CB) reveal that neonatal cells display reduced rolling fractions compared with adult CD34(+) cells obtained from peripheral blood or BM, suggesting abnormal selectin ligand function on neonatal progenitors. Flow cytometric and intravital microscopy studies suggest that this defect results from nonfunctional P-selectin ligand on a subset ( approximately 30%) of neonatal CD34(+) cells. Further analyses indicate that P-selectin glycoprotein ligand-1 (PSGL-1) is expressed in a nonfunctional form among neonatal CD34(+) cells that do not bind P-selectin and that this subset is enriched in primitive CD34(+)CD38(lo/-) progenitors. These results underscore the potential to improve homing of CB CD34(+) cells to the BM by manipulation of selectins and their ligands.

ADP-ribosyl Cyclase↗
PubMed1991

Cyclophosphamide-induced alterations of bone marrow endothelium: implications in homing of marrow cells after transplantation.

Bone marrow transplantation requires infusion of stem cells i.v. and transport of these cells to the extravascular compartment of the marrow where hemopoiesis takes place. This requires massive cellular traffic across the sinus endothelial barrier. We tested the hypothesis that the conditioning regimen given before transplantation alters the endothelium and permits the traffic of transplanted cells into the hemopoietic compartment. C57B1 mice were given cyclophosphamide i.p. in doses comparable to those used in conditioning regimens. Marrow was perfusion-fixed and studied by electron microscopy at various time after the dose. The salient feature of cyclophosphamide-induced endothelial injury was membrane instability, manifested by sloughing and vesiculation of membrane on the luminal surface. Considerable loss of membrane was associated with a reduction in the surface area of endothelium. There was also an associated loss of integrity of sinus endothelium so that mature circulating red cells, normally confined to the vascular space, could now traverse the vascular wall and appear in the hemopoietic compartment. Moreover, perisinal macrophages, normally confined to extravascular space, were now seen in the lumen. We conclude that the cytotoxic conditioning regimen, given with different objectives, may facilitate the traffic of transplanted cells into the hemopoietic compartment of the marrow.

Animals↗
PubMed2001

A unique pathway in the homing of murine multiple myeloma cells: CD44v10 mediates binding to bone marrow endothelium.

Our group recently reported that multiple myeloma (MM) cells preferentially adhere to bone marrow (BM) endothelial cells and selectively home to the BM, suggesting the involvement of specific adhesive interactions in this process. The highly regulated expression of CD44 variant isoforms (CD44v) on the MM cells makes them good candidate adhesion molecules involved in this homing. We addressed this in the 5T experimental mouse model of myeloma. Fluorescence-activated cell sorting analysis demonstrated expression of CD44v6, CD44v7, and CD44v10 on the in vivo growing 5T2MM and 5T33MM myeloma lines. Antibody blocking experiments revealed the involvement of CD44v10 in the adhesion of 5T2MM and 5T33MM cells to BM endothelial cells. Coinjection of anti-CD44v10 antibodies with the myeloma cells into syngeneic mice demonstrated a selective blocking of their BM homing which resulted in a decreased BM tumor load and serum paraprotein at the end stage of the disease. The highly restricted expression of CD44v10 on MM cells, the blocking of MM adhesion to BM endothelial cells and of homing to BM by anti-CD44v10, and the decreased BM tumor load suggest that myeloma cells home to the BM via interactions mediated by this specific region of the adhesion molecule CD44.

Animals↗
PubMed2004

Rolling of human bone-metastatic prostate tumor cells on human bone marrow endothelium under shear flow is mediated by E-selectin.

Prostate tumor cells preferentially adhere to bone marrow endothelial cells (BMECs) compared with endothelial linings from other tissue microvessels, implicating the importance of BMEC adhesion in the predilection of prostate tumor metastasis to bone. E (endothelial)-selectin, which functions as an initiator of leukocyte adhesion to target tissue endothelium, is constitutively expressed on BMECs, suggesting that prostate tumor cells could use this adhesive mechanism to initiate their migration into bone. In this report, we demonstrate for the first time that human bone-metastatic prostate tumor cells roll on human BMECs under physiological flow conditions. We show that these dynamic adhesive interactions are dependent on the expression of BMEC E-selectin and sialylated glycoconjugates on bone-metastatic prostate tumor cells. We also establish the importance of both glycoprotein(s) and glycosphingolipid structures displaying sialyl Lewis X epitopes as potential E-selectin ligands on bone-metastatic prostate tumor cells. Coexpression of sialylated glycoproteins and glycolipids on bone-metastatic prostate tumor cells triggers robust E-selectin binding activity, which is identical to that observed on human hematopoietic progenitor cells. By Western blot analysis, we identify candidate E-selectin glycoprotein ligand(s); distinct sialyl Lewis X (or HECA-452 antigen)-bearing membrane proteins were resolved at M(r) 130,000 and M(r) 220,000 as well as others ranging from M(r) 100,000 to M(r) 220,000. Immunohistochemical analysis of HECA-452 antigen expression on normal prostate tissue and on low- and high-grade prostate adenocarcinoma shows that HECA-452 antigen expression is directly associated with prostate tumor progression and may indicate acquisition of E-selectin ligand expression. These findings provide novel insight into potential adhesive mechanisms promoting hematogenous dissemination of prostate tumor cells into bone.

Adenocarcinoma↗
PubMed2005

Proangiogenic stimulation of bone marrow endothelium engages mTOR and is inhibited by simultaneous blockade of mTOR and NF-kappaB.

Most bone marrow (BM) malignancies develop in association with an angiogenic phenotype and increased numbers of endothelial cells. The molecular mechanisms involved in the modulation and recruitment of BM endothelium are largely unknown and may provide novel therapeutic targets for neoplastic diseases. We observed that angiogenic stimulation of BM endothelial cells activates mTOR and engages its downstream pathways 4E-BP1 and S6K1, which are inhibited by the mTOR-specific blockers rapamycin and CCI-779. Both mTOR blockers significantly inhibit growth factor- and leukemia-induced proliferation of BM endothelium by inducing G0/G1 cell-cycle arrest. This effect is associated with down-regulation of cyclin D1 and cdk2 phosphorylation, and up-regulation of the cdk inhibitors p27(kip1) and p21(cip1). Under conditions that reproduce the biomechanical fluidic environment of the BM, CCI-779 is equally effective in inhibiting BM endothelial-cell proliferation. Finally, simultaneous blockade of mTOR and NF-kappaB pathways synergize to significantly inhibit or abrogate the proliferative responses of BM endothelial cells to mitogenic stimuli. This study identifies mTOR as an important pathway for the proangiogenic stimulation of BM endothelium. Modulation of this pathway may serve as a valid therapeutic intervention in BM malignancies evolving in association with an angiogenic phenotype.

Adult↗
PubMed1996

Human immunodeficiency virus infection of bone marrow endothelium reduces induction of stromal hematopoietic growth factors.

The majority of human immunodeficiency virus (HIV)-seropositive patients develop bone marrow abnormalities associated with hematopoietic malfunction during the progression of disease. One important manifestation of HIV-associated hematopoietic dysfunction is that after myelosuppression, bone marrow recovery, a process known to be mediated in part by the production of stromal cell-derived hematopoietic growth factors, is impaired. We sought to test the hypothesis that bone marrow stromal cells are infected by HIV-1 in vivo and that production of certain stromal cell-derived hematopoietic growth factors is deficient as a consequence. In this report, we demonstrate that bone marrow microvascular endothelial cells (MVEC), a key element of the stroma, are the predominant cells infected by HIV (5% to 20%) in bone marrow stromal cultures obtained from 11 consecutive HIV-seropositive patients. Although HIV-infected stromal cultures enriched for MVEC constitutively express normal levels of interleukin (IL)-4, IL-6, granulocyte (G)-colony-stimulating factor (CSF), granulocyte-macrophage (GM)-CSF, tumor necrosis factor (TNF)-alpha, transforming growth factor (TGF)-beta, and Steel factor, IL-1 alpha-induced release of IL-6 and G-CSF is significantly reduced in these cultures. These observations suggest that HIV infection of bone marrow MVEC reduces the capacity of hematopoietic stroma to respond to regulatory signals that normally augment blood cell production during periods of increased demand.

Adult↗
PubMed2006

Leukemia-stimulated bone marrow endothelium promotes leukemia cell survival.

Extensive endothelial cell proliferation and marked neovascularization are the most pronounced microenvironmental changes consistently observed in the bone marrow (BM) of patients with acute lymphoblastic leukemia (ALL). It is not known whether ALL cells induce this phenotype and whether they receive critical signals from the tumor-associated BM endothelium. Here, we show that leukemia cells actively stimulate BM endothelium, promote de novo angiogenesis, and induce neovascularization in the leukemic BM. Soluble factors, present in the leukemic BM microenvironment, promote the proliferation, migration, and morphogenesis of BM endothelial cells, which are critical processes in tumor angiogenesis. We also show in vitro that leukemia cells display directional motion towards assembled BM endothelium and following adherence exhibit cell polarization, pseudopodia, and ultrastructural features that suggest the existence of leukemia-endothelium cross-talk. Finally, we show that BM endothelium promotes leukemia cell survival through a mechanism mediated through the anti-apoptotic molecule bcl-2. These studies indicate that ALL cells actively recruit BM endothelium and mediate the leukemia-associated neovascularization observed in ALL. Therefore, disruption of interactions between leukemia cells and BM endothelium may constitute a valid therapeutic strategy.

Animals↗
PubMed2000

E-selectin and very late activation antigen-4 mediate adhesion of hematopoietic progenitor cells to bone marrow endothelium.

Adhesion of CD34+ hematopoietic progenitor cells (HPCs) to sinusoidal endothelium probably plays a key role in homing of transplanted CD34+ HPCs to the bone marrow (BM). We have investigated the role of various adhesion molecules in the interaction of purified CD34+ HPCs derived from BM or peripheral blood (PB) and a human BM-derived endothelial cell line. Adhesion of CD34+ HPCs to endothelial cells was measured with the use of a double-color flow microfluorimetric adhesion assay. In this assay, adhesion is measured under stirring conditions, simulating blood flow in sinusoidal marrow vessels. Adhesion of PB CD34+ cells to human BM endothelial cells (HBMECs) was observed only after interleukin (IL)-1beta prestimulation of the endothelial cells. This adhesion was strongly increased after addition of phorbol-myristate acetate (PMA). Adhesion of PB CD34+ cells to IL-1beta-prestimulated HBMECs was inhibited by blocking monoclonal antibodies (mAbs) against E-selectin and by neuraminidase treatment of the PB CD34+ cells. mAbs against very late activation antigen (VLA)-4 inhibited adhesion only when the E-selectin-mediated interaction was prevented. No clear inhibiting effect was found with blocking mAbs against beta2-integrins. Stimulation with the beta1-integrin-activating mAb, 8A2, induced adhesion of CD34+ cells to endothelial cells. In conclusion, stimulation of both endothelial cells and CD34+ HPCs is necessary for adhesion of CD34+ HPCs to endothelial cells. We furthermore demonstrated that E-selectin and VLA-4 mediated this adhesion.

Antigens, CD34↗
PubMed1981

Structure and function of sinusoidal endothelium of bone marrow.

The endothelium of marrow sinuses is the site of cellular and molecular exchange between the circulation and the hemopoietic compartment. Here, mature cells are delivered into circulation by passing through the cytoplasm of a single endothelial cell. Similarly, stem cells are probably trapped here. The endothelium which is structurally polarized, and shows segmental surface differentiations, can maintain a gradient for a variety of substances between blood and marrow (the marrow-blood barrier). Transendothelial cell migration involves channel formation through fusion-fission reorganization of the membrane. The endothelium is involved in other interactions particularly with perisinal macrophages. Little is known of the surface characteristics of the endothelium, an area that may help the understanding of how the cell can selectively exchange cells and molecules between the marrow and blood.

Animals↗
PubMed1992

Alterations of bone marrow sinus endothelium induced by ionizing irradiation: implications in the homing of intravenously transplanted marrow cells.

The endothelium of bone marrow sinuses is a continuous layer which is selective in its cellular transport. It is not known how selective and massive seeding of hemopoietic progenitor cells after intravenous transplantation of marrow cells occurs. We postulate that the conditioning irradiation could disrupt the endothelial barrier, thus permitting the "homing" of progenitor cells to occur. To demonstrate this phenomenon, we irradiated mice with doses ranging from 100-2000 cGy-total body and studied perfusion-fixed marrow by transmission electron microscopy. The major finding was sloughing and denudation of plasma membrane, particularly on the luminal side of endothelium. Membrane vesiculation was also frequently seen in this border. Moreover, dilatation of the perinuclear space and rough endoplasmic reticulum was commonplace and testified to instability and fragility of the membrane system. Focal cytoplasmic swelling of endothelium was seen reflecting increased permissiveness of the endothelial barrier. Endocytosis and phagocytosis were increased in the marrow; and the endothelium, normally quiescent with regard to phagocytosis, was now overtly phagocytic. A dipogenecity of the adventitial layer was increased as hemopoietic function of marrow decreased. The end result of membrane alterations in the endothelium was the appearance of discontinuities in these cells, which form the essential element of bone marrow-blood barrier. Consequent to these discontinuities, the permissiveness of the endothelial barrier was enhanced and those cellular elements, such as mature, nonreticulated erythrocytes that are normally confined to the vascular space, now appeared in large number in the hemopoietic compartment. With low doses, these findings were transient and repair set in by 1-2 weeks. With higher doses, total disruption of marrow-blood barrier occurred and the process did not seem to be repairable. We conclude that the conditioning irradiation before bone marrow transplantation is essential in disrupting the endothelial barrier and permitting large-scale entry of transplanted cells into the hemopoietic compartment.

Animals↗
PubMed2004

Differential inhibition of invasion and proliferation by bisphosphonates: anti-metastatic potential of Zoledronic acid in prostate cancer.

OBJECTIVES: To determine the mode of action of Zoledronic acid in the inhibition of metastasis in prostate cancer and the reduction of prostate cancer bone metastases. METHODS: Benign and malignant primary prostatic epithelial cells (PEC) and the PC-3 prostate cancer cell line were studied in co-culture using human bone marrow stroma in the presence of escalating doses of EDTA, Clodronate, Pamidronate and Zoledronic acid. PEC binding and colony growth in bone marrow stroma was measured using standardised quantitative techniques. PEC cellular invasion through Matrigel and an endothelial monolayer was measured either in invasion chambers or by the measurement of endothelial monolayer permeability to fluorescent dextran. Co-culture supernatants were assayed for specific cytokine levels. Bone marrow cellular toxicity was assessed using a standard Mix assay. RESULTS: Treatment of PEC with up to 100 microM bisphosphonate did not affect their ability to bind to bone marrow endothelium or stroma. Bone marrow endothelial permeability was reduced by 100 microM Zoledronic acid by 3.8% (p = 0.03856). Both Pamidronate (40% at 100 microM, p < or = 0.05) and Zoledronic acid inhibited PEC invasion, with Zoledronic acid being the most potent (40% at 10 microM, p < or = 0.05 rising to 91% at 100 microM, p < or = 0.001). Zoledronic acid inhibits malignant PEC proliferation in bone marrow stroma co-culture (26.5% at 10 microM rising to 66.5% at 40 microM). This was accompanied by changes within the cytokine milieu with a >800% rise in TIMP-2. CONCLUSION: Zoledronic acid is a potent inhibitor of PEC invasion across bone marrow endothelium and colony formation with the bone marrow stroma, affecting the MMP: TIMP-2 balance to favour MMP inhibition.

Antineoplastic Agents↗
PubMed1984

Ultrastructural localization of lectin receptors on the bone-marrow sinusoidal endothelium of the rat.

The bone-marrow sinusoidal endothelium is a cellular barrier that separates developing blood cells in the extravascular space from the peripheral circulation. Mature blood elements enter the circulation via transendothelial migration pores. In the present study, monosaccharide constituents on the bone marrow endothelium were examined using lectin-affinity cytochemistry. With lectin-horseradish and lectin-ferritin conjugates, mannosyl, N-acetylglucosaminyl, galactosyl, N-acetylgalactosaminyl, and sialic acid were localized to the luminal plasmalemma, bristle-coated pits and diaphragmed fenestrae. These were conspicuously reduced on the abluminal plasmalemma. When the tissue was treated with biotinylated lectins followed by avidin-ferritin, only a localization with wheat-germ agglutinin (sialic acid; N-acetylglucosaminyl) was observed. Pretreatment of the bone marrow with neuraminidase enabled the localization of the other monosaccharide components by the biotin-avidin method. Accumulations of carbohydrate residues were identified near the endothelium subjacent to migrating cells. Fucosyl moieties marked by Ulex europaeus agglutinin ( UEA ) reagents on the endothelium were not present. All binding was abolished by incubation of tissue and lectin conjugates with specific hapten sugars. labeling was also not present after Pronase E treatment, indicating that the identified monosaccharides are components of glycoproteins rather than glycolipids. The possible function of endothelial-surface glycoproteins as receptors for the surfaces of mature blood cells and their role in transmural migration are discussed.

Animals↗
PubMed1983

Mapping of the bone marrow sinus endothelium with lectins and glycosylated ferritins: identification of differentiated microdomains and their functional significance.

The distribution of lectin binding sites and sugar-recognizing systems (lectin-like substances) was studied on the luminal side of the bone marrow sinus endothelium in rats. Ferritin-conjugated lectins (Con A, PHA, RCA, WGA, UEA) and glycosylated ferritins (mannosyl, fucosyl, chitobiosyl) were used as probes. With the exception of UEA, all lectins bound to the endothelial surface. The binding was heavier on the plasmalemma proper of the nuclear region (PP-N) compared to that of the tapered region (PP-T). Lectin mapping also identified differentiated microdomains with less or no bindings. These domains related to the transport organelles in the endothelium: luminal vesicles (LV) and diaphragmmed fenestrae (DF). The relative density of binding for these four domains demonstrated the following spectrum PP-N greater than PP-T greater than LV greater than DF. The relation of this binding pattern to the transport function of marrow sinus endothelium for various cells and molecules has been discussed. Lectin mapping also identified heavily labeled microvilli and microprojections from the membrane. These organelles may have a function in recognizing cells and molecules for the transport. The absence of binding for UEA, also absent in liver endothelium, may differentiate sinus endothelia from other endothelia. This lectin is thought to be endothelium-specific in other systems. No binding was observed with glycosylated ferritins suggesting the absence of lectin-like substances on marrow sinus endothelium.

Affinity Labels↗