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The role of CXCR7 on the adhesion, proliferation and angiogenesis of endothelial progenitor cells.

Dai X, Tan Y, Cai S, Xiong X, Wang L, Ye Q, Yan X, Ma K, Cai L - J. Cell. Mol. Med. (2011)

Bottom Line: CXC chemokine receptor 4 (CXCR4) has been considered as the unique receptor of SDF-1 and as the only mediator of SDF-1-induced biological effects for many years.However, recent studies found that SDF-1 could bind to not only CXCR4 but also CXC chemokine receptor 7 (CXCR7).These results suggested that both CXCR7 and CXCR4 are important for EPCs in response to SDF-1, indicating that CXCR7 may be another potential target molecule for angiogenesis-dependent diseases.

View Article: PubMed Central - PubMed

Affiliation: Key laboratory of Biorheological Science and Technology (Chongqing University), Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, China.

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Inhibition of SDF-1-induced proliferation of EPCs by blocking both CXCR4 and CXCR7. The proliferation of EPCs induced by SDF-1 was determined by MTT assay. (A) Dose–response of the proliferation of EPCs treated with SDF-1 (0, 1, 10 and 100 ng/ml) for 8 hrs. (B) Inhibitory effects on 10 ng/ml SDF-1-induced proliferation of EPCs with pre-treatment of either anti-CXCR4 antibody (α CXCR4), anti-CXCR7 antibody (α CXCR7), IgG control, AMD3100 or CCX733, respectively. Data are given as mean ± S.D. (*P < 0.05, **P < 0.01, versus control, ##P < 0.01, versus SDF-1).
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fig06: Inhibition of SDF-1-induced proliferation of EPCs by blocking both CXCR4 and CXCR7. The proliferation of EPCs induced by SDF-1 was determined by MTT assay. (A) Dose–response of the proliferation of EPCs treated with SDF-1 (0, 1, 10 and 100 ng/ml) for 8 hrs. (B) Inhibitory effects on 10 ng/ml SDF-1-induced proliferation of EPCs with pre-treatment of either anti-CXCR4 antibody (α CXCR4), anti-CXCR7 antibody (α CXCR7), IgG control, AMD3100 or CCX733, respectively. Data are given as mean ± S.D. (*P < 0.05, **P < 0.01, versus control, ##P < 0.01, versus SDF-1).

Mentions: The proliferation of EPCs cultured in growth factor-deprived EBM-2 medium containing 1 ng/ml, 10 ng/ml or 100 ng/ml SDF-1 was measured by MTT. As shown in Figure 6A, 10–100 ng/ml SDF-1 significantly induced EPCs’ proliferation. Because it is known that SDF-1 plays an important role in EPCs’ proliferation through CXCR4 receptor [27], the next study was to investigate the role of CXCR7 in EPCs’ proliferation. To this end, we treated SDF-1-stimulated EPCs with the antibodies and antagonists of CXCR4 or CXCR7 and then analysed their proliferation rates. MTT assay demonstrated that blocking either CXCR7 or CXCR4 could not significantly reduced the enhancement of EPC proliferation induced by SDF-1, whereas blocking both CXCR7 and CXCR4 significantly inhibited the EPC proliferation induced by SDF-1 (Fig. 6B). Thus SDF-1 enhanced EPCs proliferation is mediated by both of CXCR7 and CXCR4.


The role of CXCR7 on the adhesion, proliferation and angiogenesis of endothelial progenitor cells.

Dai X, Tan Y, Cai S, Xiong X, Wang L, Ye Q, Yan X, Ma K, Cai L - J. Cell. Mol. Med. (2011)

Inhibition of SDF-1-induced proliferation of EPCs by blocking both CXCR4 and CXCR7. The proliferation of EPCs induced by SDF-1 was determined by MTT assay. (A) Dose–response of the proliferation of EPCs treated with SDF-1 (0, 1, 10 and 100 ng/ml) for 8 hrs. (B) Inhibitory effects on 10 ng/ml SDF-1-induced proliferation of EPCs with pre-treatment of either anti-CXCR4 antibody (α CXCR4), anti-CXCR7 antibody (α CXCR7), IgG control, AMD3100 or CCX733, respectively. Data are given as mean ± S.D. (*P < 0.05, **P < 0.01, versus control, ##P < 0.01, versus SDF-1).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4373330&req=5

fig06: Inhibition of SDF-1-induced proliferation of EPCs by blocking both CXCR4 and CXCR7. The proliferation of EPCs induced by SDF-1 was determined by MTT assay. (A) Dose–response of the proliferation of EPCs treated with SDF-1 (0, 1, 10 and 100 ng/ml) for 8 hrs. (B) Inhibitory effects on 10 ng/ml SDF-1-induced proliferation of EPCs with pre-treatment of either anti-CXCR4 antibody (α CXCR4), anti-CXCR7 antibody (α CXCR7), IgG control, AMD3100 or CCX733, respectively. Data are given as mean ± S.D. (*P < 0.05, **P < 0.01, versus control, ##P < 0.01, versus SDF-1).
Mentions: The proliferation of EPCs cultured in growth factor-deprived EBM-2 medium containing 1 ng/ml, 10 ng/ml or 100 ng/ml SDF-1 was measured by MTT. As shown in Figure 6A, 10–100 ng/ml SDF-1 significantly induced EPCs’ proliferation. Because it is known that SDF-1 plays an important role in EPCs’ proliferation through CXCR4 receptor [27], the next study was to investigate the role of CXCR7 in EPCs’ proliferation. To this end, we treated SDF-1-stimulated EPCs with the antibodies and antagonists of CXCR4 or CXCR7 and then analysed their proliferation rates. MTT assay demonstrated that blocking either CXCR7 or CXCR4 could not significantly reduced the enhancement of EPC proliferation induced by SDF-1, whereas blocking both CXCR7 and CXCR4 significantly inhibited the EPC proliferation induced by SDF-1 (Fig. 6B). Thus SDF-1 enhanced EPCs proliferation is mediated by both of CXCR7 and CXCR4.

Bottom Line: CXC chemokine receptor 4 (CXCR4) has been considered as the unique receptor of SDF-1 and as the only mediator of SDF-1-induced biological effects for many years.However, recent studies found that SDF-1 could bind to not only CXCR4 but also CXC chemokine receptor 7 (CXCR7).These results suggested that both CXCR7 and CXCR4 are important for EPCs in response to SDF-1, indicating that CXCR7 may be another potential target molecule for angiogenesis-dependent diseases.

View Article: PubMed Central - PubMed

Affiliation: Key laboratory of Biorheological Science and Technology (Chongqing University), Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, China.

Show MeSH
Related in: MedlinePlus