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PubMed2002

Seasonal dynamics of flight muscle fatty acid binding protein and catabolic enzymes in a migratory shorebird.

We developed an ELISA to measure heart-type fatty acid binding protein (H-FABP) in muscles of the western sandpiper (Calidris mauri), a long-distance migrant shorebird. H-FABP accounted for almost 11% of cytosolic protein in the heart. Pectoralis H-FABP levels were highest during migration (10%) and declined to 6% in tropically wintering female sandpipers. Premigratory birds increased body fat, but not pectoralis H-FABP, indicating that endurance flight training may be required to stimulate H-FABP expression. Juveniles making their first migration had lower pectoralis H-FABP than adults, further supporting a role for flight training. Aerobic capacity, measured by citrate synthase activity, and fatty acid oxidation capacity, measured by 3-hydroxyacyl-CoA-dehydrogenase and carnitine palmitoyl transferase activities, did not change during premigration but increased during migration by 6, 12, and 13%, respectively. The greater relative induction of H-FABP (+70%) with migration than of catabolic enzymes suggests that elevated H-FABP is related to the enhancement of uptake of fatty acids from the circulation. Citrate synthase, 3-hydroxyacyl-CoA-dehydrogenase, and carnitine palmitoyl transferase were positively correlated within individuals, suggesting coexpression, but enzyme activities were unrelated to H-FABP levels.

3-Hydroxyacyl CoA Dehydrogenases↗

PubMed1999

Breast cancer and oral contraceptive use in Asian-American women.

Breast cancer incidence has historically been 4-7 times higher in the United States than in Asia. A previous study by the authors in Asian-American women demonstrated a substantial increase in breast cancer risk in women who migrated from Asia to the United States, with the risk almost doubling during the first decade after migration. Increased use of oral contraceptives soon after migration to the United States could possibly explain this rapid rise in risk. In a population-based case-control study of Chinese, Filipino, and Japanese-American women, aged 20-55 years, who lived in San Francisco-Oakland, California; Los Angeles, California; and Oahu, Hawaii during 1983-1987, 597 cases (70% of those eligible) and 966 controls (75%) were interviewed. Controls were matched to cases on age, ethnicity, and area of residence. Oral contraceptive (OC) use increased with time since migration; 15.0% of Asian-born women who had been in the West <8 years, 33.4% of Asian-born women who had been in the West > or =8 years, and 49.6% of Asian women born in the West had ever used OCs. However, duration of OC use (adjusted for age, ethnicity, study area, years since migration, education, family history of breast cancer and age at first full-term birth) was not associated with increased risk of breast cancer. Moreover, neither OC use before age 25 years nor before first full-term birth was associated with increased risk. Results were unchanged when restricted to women under age 45 years or under age 40 years. After adjustment for duration of OC use, women who had been in the United States > or =8 years were still at almost twice the risk of breast cancer compared with women who had been in the United States 2-7 years. This study suggests that OC use cannot explain the elevated risk observed in Asian women who migrated to the United States > or =7 years ago.

Adult↗

PubMed1998

Blockade of chemokine activity by a soluble chemokine binding protein from vaccinia virus.

Chemokines direct migration of immune cells into sites of inflammation and infection. Chemokine receptors are seven-transmembrane domain proteins that, in contrast to other cytokine receptors, cannot be easily engineered as soluble chemokine inhibitors. Poxviruses encode several soluble cytokine receptors to evade immune surveillance, providing new strategies for immune modulation. Here we show that vaccinia virus and other orthopoxviruses (cowpox and camelpox) express a secreted 35-kDa chemokine binding protein (vCKBP) with no sequence similarity to known cellular chemokine receptors. The vCKBP binds CC, but not CXC or C, chemokines with high affinity (Kd = 0.1-15 nM for different CC chemokines), blocks the interaction of chemokines with cellular receptors, and inhibits chemokine-induced elevation of intracellular calcium levels and cell migration in vitro, thus representing a soluble inhibitor that binds and sequesters chemokines. The potential of vCKBP as a therapeutic agent in vivo was illustrated in a guinea pig skin model by the blockade of eotaxin-induced eosinophil infiltration. a feature of allergic inflammatory reactions. Furthermore, vCKBP may enable the rational design of antagonists to neutralize pathogens that use chemokine receptors to initiate infection, such as HIV or the malarial parasite.

Animals↗

PubMed2006

Ephrin-A1 facilitates mammary tumor metastasis through an angiogenesis-dependent mechanism mediated by EphA receptor and vascular endothelial growth factor in mice.

Ephrin-A1, the prototypic ligand for EphA receptor tyrosine kinases, is overexpressed in vascularized tumors relative to normal tissue. Moreover, ephrin-A1-Fc fusion proteins induce endothelial cell sprouting, migration, and assembly in vitro, and s.c. vascular remodeling in vivo. Based on these data, we hypothesized that native, membrane-bound ephrin-A1 regulates tumor angiogenesis and progression. We tested this hypothesis using a transplantable mouse mammary tumor model. Small interfering RNA-mediated ephrin-A1 knockdown in metastatic mammary tumor cells significantly diminishes lung metastasis without affecting tumor volume, invasion, intravasation, or lung colonization upon i.v. injection in vivo. Ephrin-A1 knockdown reduced tumor-induced endothelial cell migration in vitro and microvascular density in vivo. Conversely, overexpression of ephrin-A1 in nonmetastatic mammary tumor cells elevated microvascular density and vascular recruitment. Overexpression of ephrin-A1 elevated wild-type but not EphA2-deficient endothelial cell migration toward tumor cells, suggesting that activation of EphA2 on endothelial cells is one mechanism by which ephrin-A1 regulates angiogenesis. Furthermore, ephrin-A1 knockdown diminished, whereas overexpression of ephrin-A1 elevated, vascular endothelial growth factor (VEGF) levels in tumor cell-conditioned medium, suggesting that ephrin-A1-mediated modulation of the VEGF pathway is another mechanism by which membrane-tethered ephrin-A1 regulates angiogenic responses from initially distant host endothelium. These data suggest that ephrin-A1 is a proangiogenic signal, regulating VEGF expression and facilitating angiogenesis-dependent metastatic spread.

Adenocarcinoma↗

PubMed1986

Effect of elevated temperature on human immunoglobulin synthesis, lymphokine production and lymphocyte proliferation in vitro.

Fever in infections is mediated by endogenous pyrogen, a protein inseparable from interleukin 1 (IL-1). It remains unclear what the role of fever in host defence is. We studied the effect of elevated temperature on mitogen-induced human lymphocyte stimulation in vitro. Lymphocyte proliferation, elaboration of leukocyte migration inhibiting factor (LIF) and immunoglobulin production were measured at normal and elevated temperatures. Pokeweed mitogen-(PWM) driven responses were quantitated with a plaque-forming cell assay and by measuring secreted immunoglobulins in culture medium. The responses at 38, 39 or 40 degrees C were, if anything, lower than those at 37 degrees C. The production of LIF after stimulation with PWM was not augmented at elevated temperatures. In contrast, the proliferative responses to PWM, phytohaemagglutinin (PHA) and concanavalin A (ConA) were increased at 38 degrees C. These results indicated that elevated temperature has diverse effects on mitogen-induced lymphocyte functions in vitro.

Cells, Cultured↗

PubMed2001

Ca2+-RhoA signaling pathway required for polyamine-dependent intestinal epithelial cell migration.

Expression of voltage-gated K(+) (Kv) channel genes is regulated by polyamines in intestinal epithelial cells (IEC-6 line), and Kv channel activity is involved in the regulation of cell migration during early restitution by controlling membrane potential (E(m)) and cytosolic free Ca2+ concentration ([Ca2+](cyt)). This study tests the hypothesis that RhoA of small GTPases is a downstream target of elevated ([Ca2+](cyt)) following activation of K(+) channels by increased polyamines in IEC-6 cells. Depletion of cellular polyamines by alpha-difluoromethylornithine (DFMO) reduced whole cell K+ currents [I(K(v))] through Kv channels and caused membrane depolarization, which was associated with decreases in ([Ca2+](cyt)), RhoA protein, and cell migration. Exogenous polyamine spermidine reversed the effects of DFMO on I(K(v)), E(m), ([Ca2+](cyt)), and RhoA protein and restored cell migration to normal. Elevation of ([Ca2+](cyt)) induced by the Ca2+ ionophore ionomycin increased RhoA protein synthesis and stimulated cell migration, while removal of extracellular Ca2+ decreased RhoA protein synthesis, reduced protein stability, and inhibited cell motility. Decreased RhoA activity due to Clostridium botulinum exoenzyme C(3) transferase inhibited formation of myosin II stress fibers and prevented restoration of cell migration by exogenous spermidine in polyamine-deficient cells. These findings suggest that polyamine-dependent cell migration is partially initiated by the formation of myosin II stress fibers as a result of Ca2+-activated RhoA activity.

Animals↗

PubMed1990

[DNA synthesis and content in the macrophage nuclei of normal mice, during carcinogenesis and during the administration of retinoids to the animals].

It has been found that nearly 50% of the lymph node and spleen macrophages (MP) of the CBA line mice contain DNA at levels superior to the diploid value (H2c--H4c in mononuclear MP, and up to H16c among polynuclear ones, the latter comprising 2.5-9.0% of the whole MP population). No DNA synthesis and mitosis were detected by autoradiography, cytophotometry, and cytomorphological analysis. During carcinogenesis the proportion of MP with elevated DNA amounts ("activated MPs") decreases due to their migration to tumours. Also immature MPs (1.6%) appear in the population, which synthesize DNA, but do not divide. Injection of retinoids restores the percentage of MPs with elevated DNA amounts to the levels characteristic of the intact animals, the fraction of DNA-synthetizing cells increasing up to 2.8%. It is proposed that retinoids may accelerate the processes of MP maturation, activation and renewing. A mechanism of cooperative action of MPs and retinoids is discussed in addition to the role of DNA hyper-replication.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed2005

Elevated CXCL16 expression by synovial macrophages recruits memory T cells into rheumatoid joints.

OBJECTIVE: Directional migration of leukocytes is orchestrated by the regulated expression of chemokine receptors and their ligands. The receptor CXCR6 is abundantly expressed by Th1-polarized effector/memory lymphocytes accumulating at inflammatory sites. This study was undertaken to examine the presence of CXCR6+ T cells and of CXCL16, the only ligand for CXCR6, in the joints of patients with rheumatoid arthritis (RA). METHODS: Flow cytometry analysis of the expression of CXCR6 by peripheral blood and synovial fluid (SF) T cells. In addition, by performing conventional and real-time reverse transcriptase-polymerase chain reaction, immunohistochemistry, and enzyme-linked immunosorbent assay, we determined the expression of CXCL16 and its protease ADAM-10 within synovium and by cultured macrophages. SF T cell migration was studied with the Transwell system. RESULTS: Accumulation of CXCR6+ T cells within RA SF coincided with highly elevated levels of CXCL16+ macrophages. In vitro studies revealed that monocytes started to express CXCL16 upon differentiation into macrophages, and that RA SF and tumor necrosis factor (TNF) enhanced CXCL16 expression. Moreover, RA patients responding to anti-TNF therapy showed a strongly decreased CXCL16 expression, whereas nonresponding patients did not. Interestingly, ADAM-10, a recently identified protease of CXCL16, was abundantly expressed by CXCL16+ macrophages in vitro and in RA in vivo, which resulted in increased levels of cleaved CXCL16 in RA SF relative to controls. Finally, CXCR6+ T cells from RA SF were attracted by CXCL16. CONCLUSION: These data provide evidence that enhanced production of CXCL16 in RA synovia leads to recruitment of CXCR6+ memory T cells, thereby contributing to the inflammatory cascade associated with RA pathology.

ADAM Proteins↗

PubMed2001

Elevated superoxide production by active H-ras enhances human lung WI-38VA-13 cell proliferation, migration and resistance to TNF-alpha.

Accumulating evidence has suggested that cellular production of superoxide acts as an intracellular messenger to regulate gene expression and modulate cellular activities. In this report, we set out to investigate the role of active H-ras-mediated superoxide production on tumor cell malignancy in a SV-40 transformed human lung WI-38 VA-13 cell line. Stable transfection and expression of constitutively active mutant V12-H-ras (V12-H-ras) dramatically increased intracellular production of superoxide. The expression of V12-H-ras significantly enhanced cell proliferation, migration and resistance to TNF-alpha treatment compared to that of parental and vector control cells, while expression of wild type H-ras (WT-H-ras) only had modest effects. Upon scavenging by superoxide dismutase and other molecules that decrease the intracellular level of active H-ras mediated superoxide production, cell proliferation, migration and resistance to TNF-alpha were significantly reduced. Furthermore, we demonstrated that the activation of membrane NADPH oxidase activity by expression of active H-ras contributed to the intracellular superoxide production. The causal relationship between membrane superoxide production and increased cell proliferation, migration, and resistance to TNF-alpha by the expression of active H-ras, has provided direct evidence to demonstrate that superoxide acts as an intracellular messenger to cascade ras oncogenic signal relay and to modulate tumor malignant activity.

Acetophenones↗

PubMed2003

Linked regulation of motility and integrin function in activated migrating neutrophils revealed by interference in remodelling of the cytoskeleton.

Neutrophils migrate rapidly by co-ordinating regulation of their beta2-integrin adhesion with turnover of filamentous F-actin. The seven-protein Arp2/3 complex regulates actin polymerisation upon activation by proteins of the WASP-family. To investigate links between actin polymerisation, adhesion, and migration, we used a novel osmotic-shock method to load neutrophils with peptides: (1). WASP-WA and Scar-WA (which incorporate the actin- and Arp2/3-binding regions of WASP and Scar1), to compete with endogenous WASP-family members; (2). proline rich motifs (PRM) from the ActA protein of L. monocytogenes or from vinculin, which bind vasodilator-stimulated phosphoprotein (VASP), a regulator of cytoskeleton assembly. In a flow system, rolling-adherent neutrophils were stimulated with formyl tri-peptide. This caused rapid immobilisation, followed by migration with increasing velocity, supported by activated beta2-integrin CD11b/CD18. Loading ActA PRM (but not vinculin PRM) caused concentration-dependent reduction in migration velocity. At the highest concentration, unstimulated neutrophils had elevated F-actin and were rigid, but could not change their F-actin content or shape upon stimulation. Scar-WA also caused marked reduction in migration rate, but WASP-WA had a lesser effect. Scar-WA did not modify activation-dependent formation of F-actin or change in shape. However, a reduction in rate of downregulation of integrin adhesion appeared to contribute to impaired migration. These studies show that interference in cytoskeletal reorganisation that follows activation in neutrophils, can impair regulation of integrin function as well as motility. They also suggest a role of the Arp2/3 complex and WASP-family in co-ordinating actin polymerisation and integrin function in migrating neutrophils.

Actin-Related Protein 2↗

PubMed2002

Altered phosphodiesterase 3-mediated cAMP hydrolysis contributes to a hypermotile phenotype in obese JCR:LA-cp rat aortic vascular smooth muscle cells: implications for diabetes-associated cardiovascular disease.

Cardiovascular diseases represent a significant cause of morbidity and mortality in diabetes. Of the many animal models used in the study of non-insulin-dependent (type 2) diabetes, the JCR:LA-cp rat is unique in that it develops insulin resistance in the presence of obesity and manifests both peripheral and coronary vasculopathies. In this animal model, arterial vascular smooth muscle cells (VSMCs) from homozygous obese (cp/cp) rats, but not from age-matched healthy (+/+ or + /cp, collectively defined +/?) littermates, display an " activated" phenotype in vitro and in vivo and have an elevated level of cAMP phosphodiesterase (PDE) activity. In this report, we confirm that cp/cp rat aortic VSMCs have an elevated level of PDE3 activity and show that only particulate PDE3 (PDE3B) activity is elevated. In marked contrast to results obtained in + /? VSMCs, simultaneous activation of adenylyl cyclase and inhibition of PDE3 activity in cp/cp VSMCs synergistically increased cAMP. Although PDE3 inhibition did not potentiate the antimigratory effects of forskolin on +/? VSMCs, PDE3 inhibition did markedly potentiate the forskolin-induced inhibition of migration of cp/cp-derived VSMCs. Although PDE3 activity was elevated in cp/cp rat aortic VSMCs, levels of expression of cytosolic PDE3 (PDE3A) and PDE3B in +/? and cp/cp VSMCs, as well as activation of these enzymes following activation of the cAMP-protein kinase A signaling cascade, were not different. Our data are consistent with an increased role for PDE3 in regulating cAMP-dependent signaling in cp/cp VSMCs and identify PDE3 as a cellular activity potentially responsible for the phenotype of cp/cp VSMCs.

1-Methyl-3-isobutylxanthine↗

PubMed2003

Smooth muscle cell migration stimulated by interleukin 6 is associated with cytoskeletal reorganization.

BACKGROUND: Interleukin 6 (IL-6) is elevated in the arterial wall in atherosclerosis and restenosis after angioplasty. An important contributor to these pathologies is migration of vascular smooth muscle cells (VSMC), which is often associated with cytoskeletal reorganization initiated by growth factors and chemokines. We recently reported that IL-6 stimulated migration of VSMC. Here, we examined the cytoskeleton of VSMC and cytoskeletal associated proteins to determine potential mechanisms associated with IL-6 induced migration. MATERIALS AND METHODS: Studies were performed in VSMC cultured from rat aortas. RESULTS: IL-6 significantly stimulated VSMC migration. IL-6 induced actin polymerization, and tyrosine phosphorylation of focal adhesion-associated cytoskeletal proteins including focal adhesion kinase (FAK) and paxillin. Cytochalasin D, an inhibitor of actin polymerization, blocked phosphorylation of FAK and paxillin as well as cell motility induced by the cytokine. CONCLUSIONS: Collectively, these data demonstrate for the first time that IL-6 stimulates VSMC motility which correlated with induction of actin cytoskeletal reorganization and tyrosine phosphorylation of FAK and paxillin.

Actins↗

PubMed2026

CARS1 as a Prognostic Biomarker and Candidate Therapeutic Vulnerability in Hepatocellular Carcinoma: Insights Into Tumor Progression and the Immune Microenvironment.

BACKGROUND: Cysteinyl-tRNA synthetase 1 (CARS1) has been included in ferroptosis-related prognostic signatures, but its clinicopathological relevance, cellular functions, and relationship with the immune microenvironment in hepatocellular carcinoma (HCC) remain incompletely characterized. METHODS: Transcriptomic and clinical data from The Cancer Genome Atlas Liver Hepatocellular Carcinoma (TCGA-LIHC) dataset were integrated with corresponding data from an institutional HCC tissue cohort of 60 patients. CARS1 expression was evaluated by immunohistochemistry, and immune infiltration was examined using single-sample gene-set enrichment analysis (ssGSEA) and multiplex immunofluorescence, as well as by analyzing public single-cell datasets. The effects of CARS1 depletion were evaluated in MHCC97H and Hep3B cells using Cell Counting Kit-8 (CCK-8) assays, cell-cycle profiling, wound-healing assays, Transwell migration assays, western blotting, and erlotinib-sensitivity assays. RESULTS: CARS1 expression was elevated in HCC and was associated with adverse clinicopathological features and poor overall survival. Quantitative immunohistochemistry confirmed elevated CARS1 protein expression in tumor tissues. CARS1 depletion inhibited cell proliferation, altered cell-cycle distribution, impaired migration, and enhanced in vitro sensitivity to erlotinib. High CARS1 expression was also associated with increased infiltration of Th2-like immune cells. CONCLUSIONS: Elevated CARS1 expression is associated with an adverse biological and immune phenotype in HCC. These clinical, histopathological, and loss-of-function findings support further investigation of CARS1 as a prognostic marker and candidate therapeutic target in HCC, although additional mechanistic and in vivo validation is required.

Humans↗

PubMed1998

In vitro cellular response to polypyrrole-coated woven polyester fabrics: potential benefits of electrical conductivity.

Electrically conducting polypyrrole-treated films have recently been shown to influence the morphology and function of mammalian cells in vitro. This type of polymer represents a possible alternative biomaterial for use in vascular implantation. The present study compared the in vitro biocompatibility of the five different polyester woven fabrics having increasing levels of electrical conductivity ranging from 4.5 x 10(4) to 123 omega/square with that of low density polyethylene and polydimethylsiloxane primary reference materials. Biocompatibility was measured in terms of four different types of in vitro cellular response, including (a) an indirect and (b) a direct control organotypic culture assay using endothelial cells, (c) a polymorphonuclear (PMN) cell activation study using flow-cytometric measurements of CD11/CD18 integrin molecule expression, and (d) a semiquantification of interleukin (IL)-6 mRNA expression on monocytes/macrophages using reverse-transcriptase polymerase chain reaction. The organotypic culture study revealed that the fabrics with high levels of conductivity exhibited lower cell migration, proliferation, and viability. The PMN activation study of blood from 10 healthy adult donors demonstrated that the two most conductive fabrics were able to identify the more reactive donors. The levels of IL-6 mRNA expression by monocytes/macrophages decreased as the conductivity level of the fabrics increased. The results of the present study therefore indicate that high levels of conductivity (< 200 omega/square) on polyester fabrics are detrimental to the growth, migration, and viability of endothelial cells; induce elevated PMN activation; and affect the intracellular metabolism of monocytes. They also point to a specific range of conductivity (10(3) < 10(4) omega/square) which is associated with an optimum in vitro cellular response.

Adult↗

PubMed1988

Responses of rat alveolar macrophages to inhaled brass powder.

The effects of a single acute exposure to inhaled brass dust on rat pulmonary alveolar macrophages (PAM) were determined. Pulmonary alveolar macrophages lavaged from the lungs of these experimental animals showed both morphological and functional abnormalities. Exposure to brass dust caused a rapid, transient inflammatory response, producing an influx of polymorphonuclear leukocytes into the lavage fluid. Binucleation and multinucleation of PAM were sensitive morphological indicators of pulmonary stress that persisted throughout the 14-day course of the experiment. Pulmonary alveolar macrophages from rats exposed to brass dust were phagocytically activated; both the total numbers of test particulates ingested and the phagocytic index were elevated. Chemotaxis, as measured by direct cellular migration in Boyden chambers, was inhibited for 3 days after exposure, but was markedly stimulated from 7 to 14 days. This was interpreted as a possible consequence of a selective release of lymphokines during the course of the inflammatory response. Some of these results, based on in vivo exposure of PAM to inhaled particulates, differ from those derived from in vitro exposure. This points to the fact that it is virtually impossible to duplicate the native chemical microenvironment of PAM in vitro and emphasizes the necessity of bringing about PAM-particle interactions in the intact lung in order to obtain more physiologically relevant data.

Administration, Inhalation↗

PubMed1993

Catheter-induced pulmonary artery haemorrhage resulting from a pneumothorax.

We present a case of pulmonary artery perforation in a patient who developed a pneumothorax after cardiac surgery. In the process of inserting a chest tube the patient became tachypnoeic, and developed haemoptysis. The trachea was intubated, and right bronchial intubation was performed with persistent bleeding. The pulmonary artery catheter was gently withdrawn and the balloon inflated, with cessation of bleeding. The patient was taken to the operating room, a bronchial blocker was placed in the right lower lobe bronchi, and the pulmonary artery catheter was removed. The bronchial blocker was removed the following day with no bleeding. The aetiology of perforation was secondary to the pneumothorax, which caused a shift of the mediastinum to the right, elevated pulmonary artery pressures, and the distal migration of the catheter through the pulmonary artery. It is recommended that treatment include tracheal intubation, inflation of the pulmonary artery catheter balloon, and the placement of a right lower lobe bronchial blocker.

Aged↗

PubMed2005

Growth, structure, and stability of ceria films on Si(111) and the application of CaF2 buffer layers.

The growth of ceria (CeO2) films by oxidation of evaporated Ce metal on Si(111) and on CaF2(111) epilayers on Si(111) is compared. By use of XPS, UPS, and LEED, it has been demonstrated that the application of a CaF2 buffer layer between the ceria and Si substrate prevents the formation of an amorphous oxidized Si layer at the interface and permits the growth of a well-defined epitaxial ceria layer of (111) surface orientation. The thermal stability of the CeO2/CaF2/Si(111) interface structure is limited by the solid-state reaction between CaF2 and ceria. This leads to gradual migration of fluorine into the oxide at elevated temperatures to give a solid-state solution of fluorine in the partially reduced oxide. An analysis of the composition observed after extensive annealing in a vacuum suggests that, with initial layers of CaF2 and CeO2 of similar thickness, the ultimate product may be CeOF. The onset of this solid-state reaction can, however, be significantly delayed by annealing under an oxygen atmosphere.

Journal Article↗

PubMed2002

Induction of vasculogenesis in breast cancer models.

Recently, there have been reports of postnatal vasculogenesis in cases of ischaemia models. The aim of the present study is to provide evidence of postnatal vasculogenesis in breast-cancer-bearing mice. Based on cell surface antigen expression, we isolated endothelial precursor cells from bone marrow, peripheral blood and tumour-infiltrating cells from mice that had received six human breast cancer xenografts. In all three areas (bone marrow, peripheral blood and tumour-infiltrating cells), endothelial precursor cell population was elevated in all transplanted mice. Differentiation and migration activities of endothelial precursor cells were measured by comparing levels of the endothelial precursor cell maturation markers Flk-1, Flt-1, Tie2, VE-cadherin and CD31 among these three areas. The endothelial precursor cell population was 14% or greater in the gated lymphocyte-size fraction of the inflammatory breast cancer xenograft named WIBC-9, which exhibits a hypervascular structure and de novo formation of vascular channels, namely vasculogenic mimicry (Shirakawa et al, 2001). In vitro, bone marrow-derived endothelial precursor cells from four human breast cancer xenografts proliferated and formed multiple clusters of spindle-shaped attaching cells on a vitronectin-coated dish. The attaching cells, which incorporated DiI-labelled acetylated low-density lipoprotein (DiI-acLDL) and were negative for Mac-1. The putative bone marrow derived endothelial precursor cell subset, which was double positive of CD34 and Flk-1, and comparative bone marrow derived CD34 positive with Flk-1 negative subset were cultured. The former subset incorporated DiI-acLDL and were integrated with HUVECs. Furthermore, they demonstrated significantly higher levels of murine vascular endothelial growth factor and interleukin-8 in culture supernatant on time course by enzyme-linked immunosorbent assay. These findings constitute direct evidence that breast cancer induces postnatal vasculogenesis in vivo.

Animals↗