TY - JOUR
T1 - Erratum
T2 - Mesenchymal stromal cell-derived extracellular vesicles promote myeloid-biased multipotent hematopoietic progenitor expansion via Toll-like receptor engagement (The Journal of Biological Chemistry (2016) 291 (24607-24617) DOI: 10.1074/jbc.A116.745653)
AU - Goloviznina, Natalya A.
AU - Verghese, Santhosh Chakkaramakkil
AU - Yoon, Young Me
AU - Taratula, Oleh
AU - Marks, Daniel L.
AU - Kurre, Peter
N1 - Publisher Copyright:
© 2017 by The American Society for Biochemistry and Molecular Biology, Inc.
PY - 2017/2/24
Y1 - 2017/2/24
N2 - There were several errors in the original figure legend to Fig. 4. The figure legend should be replaced with the following. FIGURE 4. MSC-derived EVs activate NF-κB and Notch signaling to promote HSPC differentiation. A, diagrammatic representation of the lentiviral vector design used to generate the NF-κB enhancer-luciferase reporter cell line. Stably transduced and sorted SIM-A9 microglial cells were used for EV exposure followed by luciferase assay. The SIM-A9-NF-κB-Luc cells were exposed with MSC EVs and incubated for 48 h followed by luciferase assay. Non-treated SIM-A9-NF-κB-Luc and LPS-treated SIM-A9-NF-κB-Luc cells were used as negative and positive controls, respectively. Luciferase activity was measured as relative fluorescence units (RFU). Data represent n = 4 independent experiments; error bars depict S.D. All p values have been calculated using two-tailed Student's t test. B, quantitative mRNA expression of NF-κB and Notch-1 signaling and downstream targets involved in cell proliferation in MSC EV-exposed HSPCs. Data represent n = 3 independent experiments; error bars are S.D. C, we next tested a candidate panel of canonical TLR4 responsive cytokines for both transcriptional activation and secretion, either after EV or S100 exposure. Transcriptional analysis of EV-exposed HSPCs reveals an up-regulation of several known TLR4-responsive cytokine genes (IL6, TNFa, Stat1, and EGFR) in WT but not MyD88-/- HSPCs. Data represent n = 3 independent experiments; error bars are S.D. D, TLR4 signaling was specifically inhibited in WT MSC-EV-exposed HSPCs using TAK-242. Transcriptional analysis of EV-exposed HSPCs with and without TLR4 inhibitor showed down-regulation of the same TLR-responsive genes described above. Data represent n = 2 independent experiments; error bars represent S.D. E, cytokines released by HSPCs after 48 h co-culture, with MSC EVs compared with S100, were measured using a Luminex assay, whereby error bars are S.D. and p values are an indication of the variance across three technical replicates in this screening panel.
AB - There were several errors in the original figure legend to Fig. 4. The figure legend should be replaced with the following. FIGURE 4. MSC-derived EVs activate NF-κB and Notch signaling to promote HSPC differentiation. A, diagrammatic representation of the lentiviral vector design used to generate the NF-κB enhancer-luciferase reporter cell line. Stably transduced and sorted SIM-A9 microglial cells were used for EV exposure followed by luciferase assay. The SIM-A9-NF-κB-Luc cells were exposed with MSC EVs and incubated for 48 h followed by luciferase assay. Non-treated SIM-A9-NF-κB-Luc and LPS-treated SIM-A9-NF-κB-Luc cells were used as negative and positive controls, respectively. Luciferase activity was measured as relative fluorescence units (RFU). Data represent n = 4 independent experiments; error bars depict S.D. All p values have been calculated using two-tailed Student's t test. B, quantitative mRNA expression of NF-κB and Notch-1 signaling and downstream targets involved in cell proliferation in MSC EV-exposed HSPCs. Data represent n = 3 independent experiments; error bars are S.D. C, we next tested a candidate panel of canonical TLR4 responsive cytokines for both transcriptional activation and secretion, either after EV or S100 exposure. Transcriptional analysis of EV-exposed HSPCs reveals an up-regulation of several known TLR4-responsive cytokine genes (IL6, TNFa, Stat1, and EGFR) in WT but not MyD88-/- HSPCs. Data represent n = 3 independent experiments; error bars are S.D. D, TLR4 signaling was specifically inhibited in WT MSC-EV-exposed HSPCs using TAK-242. Transcriptional analysis of EV-exposed HSPCs with and without TLR4 inhibitor showed down-regulation of the same TLR-responsive genes described above. Data represent n = 2 independent experiments; error bars represent S.D. E, cytokines released by HSPCs after 48 h co-culture, with MSC EVs compared with S100, were measured using a Luminex assay, whereby error bars are S.D. and p values are an indication of the variance across three technical replicates in this screening panel.
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U2 - 10.1074/jbc.M116.745653
DO - 10.1074/jbc.M116.745653
M3 - Comment/debate
C2 - 28235900
AN - SCOPUS:85013860028
SN - 0021-9258
VL - 292
SP - 3541
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
IS - 8
ER -