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Antiangiogenic Effect of Ethanol Extract of Vigna angularis via Inhibition of Phosphorylation of VEGFR2, Erk, and Akt.

Kwon OS, Jeong MS, Kim B, Kim SH - Evid Based Complement Alternat Med (2015)

Bottom Line: EVA showed weak cytotoxicity in HUVECs, while it significantly suppressed the VEGF induced proliferation of HUVECs.Of note, EVA effectively attenuated the phosphorylation of VEGFR2, Erk, and Akt in VEGF-treated HUVECs.Overall, our findings suggest that EVA inhibits angiogenesis in VEGF-treated HUVECs via inhibition of phosphorylation of VEGFR2, ERK, and Akt.

View Article: PubMed Central - PubMed

Affiliation: Department of East West Medical Science, Graduate School of East West Medical Science, Kyung Hee University, Suwon 446-701, Republic of Korea.

ABSTRACT
Though dietary azuki bean (Vigna angularis) seed containing antioxidant proanthocyanidins was known to have multibiological activities including antioxidant, hypotensive, anti-inflammatory, and immunomodulatory activities, the antiangiogenic activity of ethanol extract of Vigna angularis (EVA) was never reported so far. In the present study, the antiangiogenic mechanism of EVA was examined in human umbilical vein endothelial cells (HUVECs). EVA showed weak cytotoxicity in HUVECs, while it significantly suppressed the VEGF induced proliferation of HUVECs. Consistently, wound healing assay revealed that EVA inhibited the VEGF induced migration of HUVECs. Also, EVA abrogated the VEGF induced tube formation of HUVECs in a concentration dependent fashion. Furthermore, Matrigel plug assay showed that EVA significantly reduced the hemoglobin level of Matrigel plug in mice compared to untreated control. Of note, EVA effectively attenuated the phosphorylation of VEGFR2, Erk, and Akt in VEGF-treated HUVECs. Overall, our findings suggest that EVA inhibits angiogenesis in VEGF-treated HUVECs via inhibition of phosphorylation of VEGFR2, ERK, and Akt.

No MeSH data available.


Related in: MedlinePlus

Akt, Erk inhibitors, and EVA attenuate tube formation enhanced by VEGF in HUVECs. (a) Matrigel (250 μL) was added to 24-well plates and EVA (20 μg/mL), LY294002 (Akt inhibitor, 20 μM), and PD98059 (Erk inhibitor, 50 μM) were treated to HUVECs (1 × 105 cells/well) in the presence of VEGF (50 ng/mL) and incubated at 37°C. After 18 h, randomly chosen fields were photographed under an Axiovert S 100 light microscope. (b) Bar graph represents the quantification of tube formation of each group. Data are presented as means ± SD. ∗p < 0.05 versus VEGF-treated group.
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fig7: Akt, Erk inhibitors, and EVA attenuate tube formation enhanced by VEGF in HUVECs. (a) Matrigel (250 μL) was added to 24-well plates and EVA (20 μg/mL), LY294002 (Akt inhibitor, 20 μM), and PD98059 (Erk inhibitor, 50 μM) were treated to HUVECs (1 × 105 cells/well) in the presence of VEGF (50 ng/mL) and incubated at 37°C. After 18 h, randomly chosen fields were photographed under an Axiovert S 100 light microscope. (b) Bar graph represents the quantification of tube formation of each group. Data are presented as means ± SD. ∗p < 0.05 versus VEGF-treated group.

Mentions: To investigate the roles of Erk and Akt in angiogenesis, tube formation assay was conducted with HUVECs in the presence of LY294002 (Akt inhibitor) or PD98059 (Erk inhibitor). As shown in Figures 7(a) and 7(b), Akt, Erk inhibitors, and EVA treatments inhibited tube formation enhanced by VEGF. Particularly, LY294002 and EVA significantly attenuated the tube formation.


Antiangiogenic Effect of Ethanol Extract of Vigna angularis via Inhibition of Phosphorylation of VEGFR2, Erk, and Akt.

Kwon OS, Jeong MS, Kim B, Kim SH - Evid Based Complement Alternat Med (2015)

Akt, Erk inhibitors, and EVA attenuate tube formation enhanced by VEGF in HUVECs. (a) Matrigel (250 μL) was added to 24-well plates and EVA (20 μg/mL), LY294002 (Akt inhibitor, 20 μM), and PD98059 (Erk inhibitor, 50 μM) were treated to HUVECs (1 × 105 cells/well) in the presence of VEGF (50 ng/mL) and incubated at 37°C. After 18 h, randomly chosen fields were photographed under an Axiovert S 100 light microscope. (b) Bar graph represents the quantification of tube formation of each group. Data are presented as means ± SD. ∗p < 0.05 versus VEGF-treated group.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4556864&req=5

fig7: Akt, Erk inhibitors, and EVA attenuate tube formation enhanced by VEGF in HUVECs. (a) Matrigel (250 μL) was added to 24-well plates and EVA (20 μg/mL), LY294002 (Akt inhibitor, 20 μM), and PD98059 (Erk inhibitor, 50 μM) were treated to HUVECs (1 × 105 cells/well) in the presence of VEGF (50 ng/mL) and incubated at 37°C. After 18 h, randomly chosen fields were photographed under an Axiovert S 100 light microscope. (b) Bar graph represents the quantification of tube formation of each group. Data are presented as means ± SD. ∗p < 0.05 versus VEGF-treated group.
Mentions: To investigate the roles of Erk and Akt in angiogenesis, tube formation assay was conducted with HUVECs in the presence of LY294002 (Akt inhibitor) or PD98059 (Erk inhibitor). As shown in Figures 7(a) and 7(b), Akt, Erk inhibitors, and EVA treatments inhibited tube formation enhanced by VEGF. Particularly, LY294002 and EVA significantly attenuated the tube formation.

Bottom Line: EVA showed weak cytotoxicity in HUVECs, while it significantly suppressed the VEGF induced proliferation of HUVECs.Of note, EVA effectively attenuated the phosphorylation of VEGFR2, Erk, and Akt in VEGF-treated HUVECs.Overall, our findings suggest that EVA inhibits angiogenesis in VEGF-treated HUVECs via inhibition of phosphorylation of VEGFR2, ERK, and Akt.

View Article: PubMed Central - PubMed

Affiliation: Department of East West Medical Science, Graduate School of East West Medical Science, Kyung Hee University, Suwon 446-701, Republic of Korea.

ABSTRACT
Though dietary azuki bean (Vigna angularis) seed containing antioxidant proanthocyanidins was known to have multibiological activities including antioxidant, hypotensive, anti-inflammatory, and immunomodulatory activities, the antiangiogenic activity of ethanol extract of Vigna angularis (EVA) was never reported so far. In the present study, the antiangiogenic mechanism of EVA was examined in human umbilical vein endothelial cells (HUVECs). EVA showed weak cytotoxicity in HUVECs, while it significantly suppressed the VEGF induced proliferation of HUVECs. Consistently, wound healing assay revealed that EVA inhibited the VEGF induced migration of HUVECs. Also, EVA abrogated the VEGF induced tube formation of HUVECs in a concentration dependent fashion. Furthermore, Matrigel plug assay showed that EVA significantly reduced the hemoglobin level of Matrigel plug in mice compared to untreated control. Of note, EVA effectively attenuated the phosphorylation of VEGFR2, Erk, and Akt in VEGF-treated HUVECs. Overall, our findings suggest that EVA inhibits angiogenesis in VEGF-treated HUVECs via inhibition of phosphorylation of VEGFR2, ERK, and Akt.

No MeSH data available.


Related in: MedlinePlus