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Expression of Endothelial Cell-Associated Molecules in AML

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Expression of Endothelial Cell-Associated Molecules in AML Leukemia (2002) 16, 112–119 2002 Nature Publishing Group All rights reserved 0887-6924/02 $25.00 www.nature.com/leu Expression of endothelial cell-associated molecules in AML cells M Watarai1, H Miwa1, M Shikami1, K Sugamura1, M Wakabayashi1, A Satoh1, K Tsuboi1, A Imamura1, H Mihara1, Y Katoh1, K Kita2 and M Nitta1 1Department of Internal Medicine, Division of Hematology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan; and 2Tokura Hospital, Uji, Kyoto, Japan Recently, it has been clarified that interaction between hemato- hematopoietic cells is also mediated by adhesion molecules poietic cells and endothelial cells is important in normal hema- such as integrins, as well as soluble factors.10,11 topoiesis and leukemogenesis. In this study, we examined the relationship between AML cells and endothelial cells by analyz- Angiopoietins and VEGF are recognized to act coordinately ing the expression profile of angiogenic factors, angiopoietin- during vascular growth and remodeling. Blood vessels remain 1 (Ang-1), Ang-2, Tie-2 (a receptor for angiopoietins) and vascu- in a stable state when Tie-2 receptor is constitutively engaged lar endothelial growth factor (VEGF). Our results demonstrated with angiopoietin-1 (Ang-1) by stabilizing blood vessels -that CD7(؉)AML expressed Ang-2 mRNA frequently and inte- through interactions with perivascular cells and the extracellu grin-family adhesion molecules (CD11c and CD18) intensively, lar matrix. When Ang-2 expression is up-regulated, the inter- suggesting the close correlation with endothelial cells. On the other hand, in t(8;21) AML cells, expression of Ang-2 was action between Tie-2 and Ang-1 is disrupted, and the vessel infrequent and expression of integrin-family adhesion mol- is destabilized. Endothelial cells, separated from support cells ecules (CD11b, CD11c and CD18) was weak, suggesting the and matrix, become plastic and angiogenesis is promoted in sparse association with endothelial cells. As for CD7(؉)AML the presence of VEGF.12–15 In addition, various types of cancer cells, despite the frequent and intense expression of endo- cells have been shown to produce factors stimulating angio- thelial cell-associated molecules (such as Ang-2, CD11c and genesis in the tumor.16,17 Inhibitors for these angiogenicfac- CD18), intensity of Tie-2 expression was quite low (P < 0.05). ؉ tors are now considered to be candidates for novel therapeutic Ang-2 expressed in CD7( )AML cells is not considered to act in 18,19 an autocrine fashion, but to work on endothelial cells to ‘feed’ tools for cancer. leukemic cells. Although Ang-2 is recognized as a natural In this study, we would like to clarify the relationship antagonist for Tie-2, our data presented here suggested the between AML cells and endothelial cells by analyzing the alternative role of Ang-2 in the relationship between endothelial expression profile of angiogenicfactors,Ang-1, -2, Tie-2 and cells and leukemia cells, at least in a subset of leukemia such VEGF. Phenotype- and karyotype-specific expression pattern as CD7(؉)AML. These results were supported by the study using AML cell lines, KG-1 (CD7 negative) and its subline KG- was observed. In addition, expression of integrin-family 1a (CD7 positive); KG-1 had mRNA expression profile of Ang- adhesion molecules also showed distinct pattern. Co-culture -1؉Ang-2−Tie-2+, while KG-1a showed Ang-1؉Ang-2؉Tie-2؊. experiment of AML cells and human umbilical vein endo These difference in the expression profile of angiogenic factors thelial cells was done to investigate the functional interaction .between CD7(؉)AML and t(8;21)AML may explain the charac- between AML cells and endothelial cells teristic morphological features of these leukemias (CD7(؉)AML as blastic type and t(8;21)AML as differentiative type). Leukemia (2002) 16, 112–119. DOI: 10.1038/sj/leu/2402326 Keywords: AML; angiopoietins; VEGF; endothelial cell Materials and methods Samples and cell lines Introduction Bone marrow (BM) and peripheral blood (PB) smears were Recently, it has been clarified that hematopoietic stem cells prepared for May–Gru¨nwald Giemsa, peroxidase, naphthol and endothelial cells originated from common precursor cell, AS-D chloroacetate esterase, and ␣-naphthyl butylate esterase hemangioblast.1–3 In the normal developmental process, inter- staining. The morphological diagnosis of AML was made action between hematopoietic stem cells and endothelial cells according to FAB classification. Karyotypic analysis was per- is thought to be important.4–6 Endothelial cells have been formed on aspirated BM cells. All samples contained more shown to produce many cytokines known to play a role in than 80% leukemic cells morphologically. All patients gave the proliferation and differentiation of hematopoieticprogeni- their informed consent for the procedure involved. Leukemic tors.4,5 Conversely, it has been shown that hematopoieticstem cells from 36 AML patients including 12 M1, 12 M2, three cells play important roles for angiogenesis.6 In addition, some M3, five M4 and four M5 cases were studied. In addition, 375 reports suggested that leukemia cells also have intimate AML samples were studied for phenotypical study, especially correlation with endothelium in bone marrow. Increased angi- of integrin-family adhesion molecules. An AML cell line, KG- ogenesis was seen in the bone marrow of acute and chronic 1 and its subline, KG-1a (provided from Cell Resource Center leukemia patients, where some angiogenic factors such as vas- for Biomedical Research, Institute of Development, Aging and cular endothelial growth factor (VEGF) and basic fibroblast Cancer, Tohoku University, Japan) were also studied. growth factor (bFGF) were implicated to be mediators.7–9 The interaction between endothelial cells and normal or malignant Cell separation Mononuclear cells (MNC) were separated from Correspondence: H Miwa, Department of Internal Medicine, Division of Hematology, Aichi Medical University School of Medicine, heparinized PB and BM by Ficoll–Hypaque centrifugation. Nagakute, Aichi, 480–1195, Japan; Fax: 81 561 63 3401 Stocked samples, which had been isolated and frozen at Received 28 May 2001; accepted 28 August 2001 −196°C in RPMI 1640 medium with 20% heat-inactivated Relationship between AML cells and endothelial cells M Watarai et al 113 fetal calf serum (FCS) and 10% dimethyl sulfoxide, were also VEGF; 1 min at 94°C, 1 min at 60°C, 2 min at 72°C (23 cycles) used as needed. for ␤-actin. In each experiment, these cycles were preceded by 10 min incubation at 95°C to activate the AmpliTaq GOLD (Roche Molecular Systems, Branchburg, NJ, USA), and fol- Immunophenotyping lowed by 7 min of 72°C for final extension. Primers for PCR are listed in Table 1.12,22–25 Products of RT-PCR, electrophor- Before immunostaining, MNC were treated with 1 mg/ml esed in 3.5% agarose, were stained with ethidium bromide human ␥-globulin for blocking of the binding due to receptors and visualized by UV light. The intensity of the band was for immunoglobulin G (IgG) Fcportion (Fc ␥R). CD13 calculated by densitometer. (recognized by My7, Coulter, Hialeah, FL, USA), and CD33 (by My9, Coulter) were tested as myeloid differentiation mark- ers. CD7 (by M-T701, PharMingen, San Diego, CA, USA) and Cell culture CD19 (by HIB19, PharMingen) were tested as lymphoid asso- ciated markers. CD34 (by HPCA-1, Becton Dickinson, Moun- Human umbilical vein endothelial cells (1.5 × 104) tain View, CA, USA) was examined as stem cell marker. (HUVEC)/cm2 culture dish were plated, then after 2 days, leu- CD11b (by Leu15, Becton Dickinson), CD11c (by B-ly6, kemia cells (4.0 × 105 cells/ml) were added on the culture. PharMingen), and CD18 (by 7E4, Immunotech, Marseille, Simple culture of leukemia cells was started simultaneously. France) were tested as integrin-family adhesion molecules. Fluorescein isothiocyanate (FITC)-conjugated goat anti-mouse immunoglobulins was used as the second reagent. Samples Table 1 The primers for PCR were examined by a flowcytometer (FACSCalibur; Nippon Becton Dickinson, Tokyo, Japan). We focused on the leu- Ref. kemic cell fraction of the cytogram to clarify its phenotype, as previously described.20 At least 5000 cells were examined Angiopoietin-1 sense 5Ј-AGTCCAGAAAACAGTGGGAG-3Ј 22 in the surface marker study. The whole mouse Igs, IgG1, and antisense 5Ј-AGCAGCTGTATCTCAAGTCG-3Ј IgG2 used as the controls were from Chemicon International (Temecula, CA, USA). Angiopoietin-2 sense 5Ј-AAGAGCATGGACAGCATAGG-3Ј 12 antisense 5Ј-GAGTGTTCCAAGAGCTGAAG-3Ј Reverse transcription-polymerase chain reaction (RT- Tie-2 PCR) sense 5Ј-CTGCAGTGCAATGAAGCATG-3Ј 23 antisense 5Ј-TGAAGGGCTTTTCCACCATC-3Ј Expression of angiopoietin-1, 2 (Ang-1, 2), Tie-2, and vascular VEGF endothelial growth factor (VEGF) and ␤-actin genes was sense 5Ј-TCGGGCCTCCGAAACCATGA-3Ј 24 detected by the reverse transcription polymerase chain reac- antisense 5Ј-CCTGGTGAGAGATCTGGTTC-3Ј tion (RT-PCR) method as previously described.21 PCR was per- ␤-actin formed by using cDNA reverse-transcribed from 200 ng of sense 5Ј-GTGGGGCGCCCCAGGCACCA-3Ј 25 total RNA in the following conditions: 1 min at 94°C, 2 min antisense 5Ј-GTCCTTAATGTCACGCACGATTTC-3Ј at 60°C, 2 min at 72°C (27 cycles) for Ang-1, 2, Tie-2 and Figure 1 RT-PCR of angiopoietin-1, -2, Tie-2, and VEGF in various AML cells. FAB subtypes are demonstrated in the uppermost case. Lower cases show the presence or absence of CD7 antigen expression or t(8;21) chromosome abnormality. RT-PCR of ␤-actin showed that the equal amount of RNA was loaded. Leukemia Relationship between AML cells and endothelial cells M Watarai et al 114 Figure 2 Expression of RNA for angiopoietin-1, -2, Tie-2 and VEGF in association with CD7 or t(8;21). Left panels (a, c, e, g) show the comparisons of RNA expression between CD7(+) AML and CD7(−) AML. Right panels (b, d, f, h) shows the comparison between t(8;21)(+)AML and t(8;21)(−) AML.
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