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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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Requirement of CXCR4 but not CXCR7 for SDF-1-induced migration of EPCs. EPC migration was assayed in 24-transwell culture plates containing microporous (8.0 μM) membranes. (A) Dose–response assay, for which EPCs suspended in EBM-2 medium supplemented with 0.5% BSA were added to the top chamber, and SDF-1 was added to the low chamber at a concentrations of 0, 1, 10 and 100 ng/ml in EBM-2 medium supplemented with 1% FBS. (B) Effect of CXCR7 or CXCR4 inhibition on the SDF-1-induced migration of EPCs, for which EPCs suspended in the above mentioned medium were added to the top chamber in presence of anti-CXCR4 antibody (α CXCR4), anti-CXCR7 antibody (α CXCR7), IgG control, AMD3100 or CCX733, and SDF-1 at a concentration of 10 ng/ml in EBM-2 medium supplemented with 1% FBS was added to the low chamber. Results are given as mean ± S.D. of three independent experiments (*P < 0.05; **P < 0.01, versus control; #P < 0.05, ##P < 0.01, versus SDF-1).
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fig04: Requirement of CXCR4 but not CXCR7 for SDF-1-induced migration of EPCs. EPC migration was assayed in 24-transwell culture plates containing microporous (8.0 μM) membranes. (A) Dose–response assay, for which EPCs suspended in EBM-2 medium supplemented with 0.5% BSA were added to the top chamber, and SDF-1 was added to the low chamber at a concentrations of 0, 1, 10 and 100 ng/ml in EBM-2 medium supplemented with 1% FBS. (B) Effect of CXCR7 or CXCR4 inhibition on the SDF-1-induced migration of EPCs, for which EPCs suspended in the above mentioned medium were added to the top chamber in presence of anti-CXCR4 antibody (α CXCR4), anti-CXCR7 antibody (α CXCR7), IgG control, AMD3100 or CCX733, and SDF-1 at a concentration of 10 ng/ml in EBM-2 medium supplemented with 1% FBS was added to the low chamber. Results are given as mean ± S.D. of three independent experiments (*P < 0.05; **P < 0.01, versus control; #P < 0.05, ##P < 0.01, versus SDF-1).

Mentions: The chemotactic activity of SDF-1 on EPCs was evaluated in vitro. SDF-1 induced the migration of EPCs in a dose-dependent manner, and 10–100 ng/ml SDF-1 can significantly induce the migration of EPCs (Fig. 4A). Pre-treatment with CXCR4 antibody or antagonist significantly inhibited SDF-1-induced EPC migration (109.7 ± 16.12% or 105.67 ± 14.11%versus 183.5 ± 17.01%, P < 0.01), whereas pre-treatment of EPCs with CXCR7 antibody or antagonist had no such effect on the chemotactic response (Fig. 4B). Blocking both CXCR7 and CXCR4 either with their antibodies or antagonists inhibited the migration of EPCs in a similar level to blocking CXCR4 alone (Fig. 4B). The results suggest that SDF-1-induced chemotactic response of EPCs was mainly mediated through 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)

Requirement of CXCR4 but not CXCR7 for SDF-1-induced migration of EPCs. EPC migration was assayed in 24-transwell culture plates containing microporous (8.0 μM) membranes. (A) Dose–response assay, for which EPCs suspended in EBM-2 medium supplemented with 0.5% BSA were added to the top chamber, and SDF-1 was added to the low chamber at a concentrations of 0, 1, 10 and 100 ng/ml in EBM-2 medium supplemented with 1% FBS. (B) Effect of CXCR7 or CXCR4 inhibition on the SDF-1-induced migration of EPCs, for which EPCs suspended in the above mentioned medium were added to the top chamber in presence of anti-CXCR4 antibody (α CXCR4), anti-CXCR7 antibody (α CXCR7), IgG control, AMD3100 or CCX733, and SDF-1 at a concentration of 10 ng/ml in EBM-2 medium supplemented with 1% FBS was added to the low chamber. Results are given as mean ± S.D. of three independent experiments (*P < 0.05; **P < 0.01, versus control; #P < 0.05, ##P < 0.01, versus SDF-1).
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4373330&req=5

fig04: Requirement of CXCR4 but not CXCR7 for SDF-1-induced migration of EPCs. EPC migration was assayed in 24-transwell culture plates containing microporous (8.0 μM) membranes. (A) Dose–response assay, for which EPCs suspended in EBM-2 medium supplemented with 0.5% BSA were added to the top chamber, and SDF-1 was added to the low chamber at a concentrations of 0, 1, 10 and 100 ng/ml in EBM-2 medium supplemented with 1% FBS. (B) Effect of CXCR7 or CXCR4 inhibition on the SDF-1-induced migration of EPCs, for which EPCs suspended in the above mentioned medium were added to the top chamber in presence of anti-CXCR4 antibody (α CXCR4), anti-CXCR7 antibody (α CXCR7), IgG control, AMD3100 or CCX733, and SDF-1 at a concentration of 10 ng/ml in EBM-2 medium supplemented with 1% FBS was added to the low chamber. Results are given as mean ± S.D. of three independent experiments (*P < 0.05; **P < 0.01, versus control; #P < 0.05, ##P < 0.01, versus SDF-1).
Mentions: The chemotactic activity of SDF-1 on EPCs was evaluated in vitro. SDF-1 induced the migration of EPCs in a dose-dependent manner, and 10–100 ng/ml SDF-1 can significantly induce the migration of EPCs (Fig. 4A). Pre-treatment with CXCR4 antibody or antagonist significantly inhibited SDF-1-induced EPC migration (109.7 ± 16.12% or 105.67 ± 14.11%versus 183.5 ± 17.01%, P < 0.01), whereas pre-treatment of EPCs with CXCR7 antibody or antagonist had no such effect on the chemotactic response (Fig. 4B). Blocking both CXCR7 and CXCR4 either with their antibodies or antagonists inhibited the migration of EPCs in a similar level to blocking CXCR4 alone (Fig. 4B). The results suggest that SDF-1-induced chemotactic response of EPCs was mainly mediated through 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