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a Department of Microbiology/Immunology, The Walther Oncology Center, Indiana University School of Medicine, Indianapolis, Indiana, USA;
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b Walther Cancer Institute, Indianapolis, Indiana, USA
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( H7 G+ t5 n9 \& Q' @Key Words. Embryonic stem cells ? SDF-1/CXCL12 ? Apoptosis ? Chemotaxis ? Differentiation
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9 u0 i) J' n( o8 \Correspondence: Hal E. Broxmeyer, Ph.D., Walther Oncology Center, Indiana University School of Medicine, 1044 West Walnut Street, R4-302, Indianapolis, Indiana 46202, USA. Telephone: 317-274-7510; Fax: 317-274-7592; e-mail: hbroxmey@iupui.edu( R# X$ B; m0 F* M9 R9 P6 U
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ABSTRACT
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1 | O" E9 w- i. FStromal cell–derived factor-1 (SDF-1/CXCL12), a CXC chemokine, was originally cloned from bone marrow (BM) stromal cells and later found to be a pre–B-cell stimulation factor . Most chemokines bind more than one receptor, and many receptors are bound by multiple chemokines. SDF-1/CXCL12 is one of the few chemokines that binds only to one receptor, CXCR4. Both SDF-1/CXCL12–/– and CXCR4–/– knockout mice share the same phenotype and die in utero with severe abnormalities in B lymphopoiesis and myelopoiesis in BM, cardiogenesis, and vascular and cerebellar development, substantiating the one chemokine–one receptor model for SDF-1/CXCL12–CXCR4 . These gene-knockout studies, in addition to other in vivo and in vitro analyses, implicated SDF-1/CXCL12 in chemotaxis and migration of hematopoietic stem cells (HSCs) and myeloid progenitor cells (MPCs) . Our previous studies showed that SDF-1/CXCL12 enhanced survival/antiapoptosis of human BM and cord blood (CB) CD343 and CD34 cells, murine and human BM MPCs, and human growth factor–dependent MO7e cells . Moreover, murine MPCs expressing an SDF-1/CXCL12 transgene under a Rous sarcoma virus promoter demonstrated enhanced survival and reduced apoptosis compared with wild-type control MPCs . These SDF-1/CXCL12 survival–enhancing effects were mediated through CXCR4 and Gi proteins, as determined by use of species-specific antibodies for mouse or human CXCR4, by the antagonist AMD3100, which blocks binding and intracellular signaling initiated by SDF-1/CXCL12 at both the mouse or human CXCR4 receptor, and by sensitivity to pertusis toxin .% c$ y- b2 y/ s( I" ]. h$ x
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In the process of evaluating factors that influence SDF-1/CXCL12 actions, we identified CD26/dipeptidylpeptidase IV (DPPIV), a membrane-bound N-terminal ectopeptidase able to cleave SDF-1/CXCL12 , as a regulatory cell surface antigen . CD26 truncated SDF-1/CXCL12 and inactivated the chemotaxis-inducing activity of SDF-1/CXCL12 for CD34 human MPCs and for Sca1 Lin– mouse BM cells . Truncated SDF-1/CXCL12 blocked the chemotaxis-inducing activity of full-length SDF-1/CXCL12 for human CD34 MPCs . SDF-1/CXCL12 cleavage by CD26/DPPIV on HSCs and MPCs acts as a regulatory event for mobilization, migration, homing, and engraftment of HSCs and MPCs and may also be involved in SDF-1/CXCL12–enhanced survival of these cells.# I2 E1 ?4 O; Q, w9 F
# H0 Q. L: n* uEmbryonic stem cells (ESCs) are pluripotent cells derived from the inner cell mass . They are capable of undergoing unlimited numbers of symmetrical divisions without differentiation; in addition, they can give rise to differentiated cell types that are derived from all three primary germ layers of the embryo . In embryonic development, the first hematopoietic and endothelial cells are derived from a common mesodermal precursor, the hemangioblast . Little is known about the effect of SDF-1/CXCL12 on regulation of ESC survival/antiapoptosis, hemangioblast formation, and differentiation. Because SDF-1/CXCL12–/– and CXCR4–/– knockout mice die at E17.5 and suffer major organ developmental abnormalities , we studied the effects of SDF-1/CXCL12 and CXCR4 on survival/apoptosis, chemotaxis, and differentiation of murine ESCs.
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/ |' y8 o1 U8 V. a% `MATERIALS AND METHODS2 v7 o6 [ z& l$ Q o& h7 N6 Y; Q% O
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Analysis of SDF-1/CXCL12 Release and CXCR4 Expression in ESCs and EBs
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To determine whether SDF-1/CXCL12 might play a role in ESC growth and survival and EB formation, we evaluated ESC lines for production/secretion of SDF-1/CXCL12 and CXCR4 expression. Both day-0 undifferentiated E14 and CCE ESCs and day-1 and -2 Ebs generated low levels of SDF-1/CXCL12 (Figs. 1A, 1B). After day 2, the levels of SDF-1/CXCL12 in the culture media increased and reached maximum on day 3, after which the levels decreased. Before normalization by cell number, the concentration of SDF-1/CXCL12 in the supernatant increased to day-3 EBs and remained at that level until day 6. Analysis of cultures of E14 ESCs demonstrated that cells that formed within EBs expressed mRNA for CXCR4 (Table 1) and expressed surface CXCR4 protein (Fig. 1C). Expression of CXCR4 started to increase in day-4 EBs, peaked at day 5, and then declined but remained elevated. Figure 1D shows dot plots of CXCR4 expression by flow cytometry. Both CXCR4 and CXCR4– undifferentiated ESCs (at day 0) highly expressed Oct-4 (Fig. 1E), which indicates that the ESCs are undifferentiated at that time.
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4 Q. e. R2 ~: L- iFigure 1. ESC/EB cell release of SDF-1/CXCL12 and CXCR4 expression. SDF-1/CXCL12 secretion from day 0 to day 6 differentiation of (A) E14 and (B) CCE ESC lines as measured by enzyme-linked immunosorbent assay. Results are shown as mean ± SD for four (CCE cell line) and five (E14 cell line) experiments, each assessed in triplicate. (C): CXCR4 surface protein expression for E14 cells as determined by flow cytometry. Day 0 represents the population of undifferentiated cells, with the days shown on the x-axis indicating days of EB cell differentiation. (D): Dot plot for CXCR4 expression: (a) isotype control, (b) day-0 ESCs, and (c) day-2 EBs. (E): Oct-4 expression of CXCR4 and CXCR4– cells: (a) isotype control and (b) day-0 ESCs. Significant increase for (A, B, and D) compared with day-0 ESCs, *p
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/ ^' S. H% ?7 m0 nTable 1. CXCR4 mRNA expression of E14 cells from days 0–6 as determined by real-time polymerase chain reaction
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Influence of SDF-1/CXCL12 on ESC Survival and Apoptosis
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1 B+ P5 L/ U6 b/ A V( MBecause ESCs release SDF-1/CXCL12 and express CXCR4, albeit at low levels, we hypothesized that SDF-1/CXCL12 would enhance survival of ESC colony formation and would demonstrate antiapoptosis activity on ESCs in suspension culture. To test this hypothesis, we assessed the effects of SDF-1/CXCL12, the CXCR4 antagonist AMD3100, and the combination of SDF-1/CXCL12 and AMD3100 on the survival of ESC colony formation subjected to delayed addition of serum but maintained in the presence of LIF (Fig. 2A). Exogenous SDF-1/CXCL12 enhanced survival of ESC colony-forming cells subjected to delayed addition of serum throughout the 4-day culture period. Antagonism of the CXCR4 receptor by AMD3100 decreased survival of ESC colonies in the absence and presence of exogenously added SDF-1/CXCL12. After counting, collected ESCs highly expressed Oct-4 demonstrating the undifferentiated nature of these cells (Fig. 2B). We next tested the effects of SDF-1/CXCL12, AMD3100, and SDF-1/CXCL12 plus AMD3100 on apoptosis of ESCs in suspension culture with LIF without addition of serum by assessing the percentage of Annexin V–positive cells (Fig. 3A). Withdrawal of serum induced apoptosis, but the presence of SDF-1/CXCL12 decreased serum withdrawal–induced apoptosis. AMD3100 enhanced apoptosis in the absence and presence of SDF-1/CXCL12. After withdrawal of serum for 4 days, ESCs still highly expressed Oct-4 (Fig. 3B). The AMD3100 results in Figures 2 and 3 suggest that endogenously produced SDF-1/CXCL12 enhances survival of ESC colony-forming cells and antiapoptosis of ESCs subjected to serum withdrawal. Moreover, exogenously added SDF-1/CXCL12 enhances survival above that of the SDF-1/CXCL12 produced by the ESCs themselves.
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1 l5 {3 K8 d: u# MFigure 2. Influence of SDF-1/CXCL12 on survival of ESC colony formation subjected to delayed addition of serum. (A): E14 ESCs were cultured without serum, and serum added at day 0, 1, 2, or 4 after the start of culture. Colonies formed by ESCs were counted 7 days after the addition of serum. Results shown are the average of three experiments, each assessed in triplicate. Experimental points were compared with the time 0 of the control group: (a) p , Z1 D4 t; D, b/ r# n9 [" a
/ [/ k/ Z" Q+ u) J/ [+ U/ |! z7 ^Figure 3. Influence of SDF-1/CXCL12 on apoptosis of ESCs subjected to serum withdrawal. (A): E14 ESCs were cultured without serum. Cells were collected at day 1, 2, 3, or 4 after serum withdrawal. Cells were stained with Annexin V: (a) p
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8 p/ ~* _/ n9 c& c+ P j& OThe SDF-1/CXCL12–CXCR4 axis is important for homing and engraftment for HSCs . Because ESCs express CXCR4, we hypothesized that SDF-1/CXCL12 could act as a chemotactic agent for ESCs. Based on our previous studies demonstrating a role for CD26 in affecting the activity of SDF-1/CXCL12 by cleaving SDF-1 and generating a SDF-1/CXCL12 antagonist of migration , we evaluated CD26 expression on ESCs hypothesizing that if CD26 were present on ESCs, that it might influence the chemotactic activity of SDF-1/CXCL12 for ESCs. We observed CD26 mRNA in ESCs by real-time RT-PCR (data not shown) and noted dim surface expression of CD26 protein (Fig. 4A). SDF-1/CXCL12 induced chemotaxis of ESCs in a characteristic dose-dependent, bell-shaped manner with maximal chemotactic response seen at 400–600 ng/ml SDF-1/CXCL12 (Fig. 4B). Little or no migration to the bottom chamber is noted with 400 ng/ml SDF-1/CXCL12 in the upper and bottom, or upper chamber only, demonstrating that SDF-1/CXCL12 is chemotactic rather than chemokinetic for ESCs. Pretreatment of ESCs with AMD3100 blocked the chemotactic response of ESCs, substantiating that SDF-1/CXCL12–induced chemotaxis was mediated through CXCR4. Pretreatment of ESCs with the CD26 inhibitor diprotin A (Fig. 4B) greatly enhanced SDF-1/CXCL12–induced chemotaxis of ESCs, suggesting that CD26 on murine ESCs plays a negative role in SDF-1/CXCL12–induced chemotaxis, consistent with the reported results in CB and adult BM stem/progenitor cells .+ C/ i3 G: H! \% z) d s6 [
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Figure 4. CD26 expression and chemotaxis of ESCs. (A): CD26 surface expression of E14 ESCs was determined by flow cytometry. The Geo mean for isotype is 2.65 verses the 6.87 for the CD26 stain. All ESCs expressed dim levels of CD26. (B): Chemotaxis assays were performed comparing diprotin A–treated () and AMD3100-treated () and nontreated () ESCs. These are the combined results of two to four experiments. t-tests were performed between and (a, p
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Effects of SDF-1/CXCL12 on ESC-Derived Hemangioblast and Primitive and Definitive Colony Formation
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! J% b5 x& Y; R; Z8 s, f2 t# t9 E ?To further evaluate hematopoietic cell differentiation of EB cells, we assessed effects of SDF-1/CXCL12 and/or AMD3100 on hemangioblasts, as well as on primitive and definitive progenitors produced in EBs. Neither SDF-1/CXCL12 nor AMD3100 had an effect on EB production of hemangioblasts (Fig. 5A). A representative hemangioblast colony is shown in Figure 5B. The hemangioblast nature of the colonies was substantiated by expression of Flk-1 and Scl but not brachyury (Fig. 5C) . However, SDF-1/CXCL12 enhanced colony formation of p-BFU-E, d-BFU-E, d-CFU-GM, and d-CFU-GEMM progenitors (Fig. 6). AMD3100 significantly decreased colony formation of these EB-produced primitive and definitive progenitor cells in the presence or absence of exogenously added SDF-1/CXCL12. This suggests that endogenous SDF-1/CXCL12 has an enhancing effect on EB production of primitive and definitive progenitors, which can be further increased by exogenously added SDF-1/CXCL12, and that the SDF-1/CXCL12 effects are mediated through CXCR4.( \3 q! T5 w) x# b2 f- x
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Figure 5. Effects of SDF-1/CXCL12 on embryonic stem cell–derived hemangioblasts. (A): E14 embryoid bodies were dissociated and plated into hemangioblast cultures. Hemangioblast colonies were scored 4 days later. Colony numbers were divided by control group number to determine fold change of control. Experiments were done in triplicate and three independent experiments averaged. (B): The colony shown is a representative hemangioblast. (C): Hemangioblast colonies were collected and checked for expression of Flk-1, Scl, and brachyury markers. Abbreviation: SDF-1/CXCL12, stromal cell–derived factor-1.
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3 U) T v w; WFigure 6. Effects of SDF-1/CXCL12 on embryonic stem cell colony formation. E14 embryoid bodies were dissociated at day 6 and plated under different culture conditions as shown. p-BFU-E was scored 5 days later, whereas CFU-GM, CFU-GEMM, and d-BFU-E were scored 7 days later. Three independent experiments were done, each in triplicate. Colony numbers were divided by control group number to obtain the fold change from control: (a) p
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DISCUSSION
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This work was supported by U.S. Public Health Service Grants RO1 HL56416, RO1 HL67384, RO1 DK53674 (to H.E.B.), and HL69669 (to L.M.P.) from the National Institutes of Health.
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4 ?8 ^5 s7 i3 TDISCLOSURES6 U" S) V9 Q9 Y" [8 o# a3 n7 U
# e B( F) v- e$ o1 q, ]The authors indicate no potential conflicts of interest./ r O" l0 v# j
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