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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

EVA effectively attenuates the phosphorylation of VEGFR2, Erk, and Akt in VEGF-treated HUVECs. Cells were treated with 10 or 20 μg/mL of EVA in the presence of VEGF for 20 h and lysed in RIPA buffer. (a) The cell lysates were prepared and subjected to Western blotting for p-VEGFR2, VEGFR2, p-Akt, Akt, p-Erk, Erk, and β-actin. (b) Bar graphs represent fold change between actin and p-VEGFR2, p-Akt, or p-Erk groups.
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fig6: EVA effectively attenuates the phosphorylation of VEGFR2, Erk, and Akt in VEGF-treated HUVECs. Cells were treated with 10 or 20 μg/mL of EVA in the presence of VEGF for 20 h and lysed in RIPA buffer. (a) The cell lysates were prepared and subjected to Western blotting for p-VEGFR2, VEGFR2, p-Akt, Akt, p-Erk, Erk, and β-actin. (b) Bar graphs represent fold change between actin and p-VEGFR2, p-Akt, or p-Erk groups.

Mentions: Since Dr. Judah Folkman suggested the importance of tumor angiogenesis, a variety of angiogenesis related factors such as VEGF, bFGF, PDGF, angiopoietin, and transforming growth factor-β (TGF-β) were studied for years [1, 43]. To elucidate antiangiogenic molecular mechanism of EVA, Western blot analysis was performed in VEGF-treated HUVECs. As shown in Figure 6, EVA effectively attenuated the phosphorylation of VEGFR2 and Erk and Akt in VEGF-treated HUVECs.


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)

EVA effectively attenuates the phosphorylation of VEGFR2, Erk, and Akt in VEGF-treated HUVECs. Cells were treated with 10 or 20 μg/mL of EVA in the presence of VEGF for 20 h and lysed in RIPA buffer. (a) The cell lysates were prepared and subjected to Western blotting for p-VEGFR2, VEGFR2, p-Akt, Akt, p-Erk, Erk, and β-actin. (b) Bar graphs represent fold change between actin and p-VEGFR2, p-Akt, or p-Erk groups.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig6: EVA effectively attenuates the phosphorylation of VEGFR2, Erk, and Akt in VEGF-treated HUVECs. Cells were treated with 10 or 20 μg/mL of EVA in the presence of VEGF for 20 h and lysed in RIPA buffer. (a) The cell lysates were prepared and subjected to Western blotting for p-VEGFR2, VEGFR2, p-Akt, Akt, p-Erk, Erk, and β-actin. (b) Bar graphs represent fold change between actin and p-VEGFR2, p-Akt, or p-Erk groups.
Mentions: Since Dr. Judah Folkman suggested the importance of tumor angiogenesis, a variety of angiogenesis related factors such as VEGF, bFGF, PDGF, angiopoietin, and transforming growth factor-β (TGF-β) were studied for years [1, 43]. To elucidate antiangiogenic molecular mechanism of EVA, Western blot analysis was performed in VEGF-treated HUVECs. As shown in Figure 6, EVA effectively attenuated the phosphorylation of VEGFR2 and Erk and Akt in VEGF-treated HUVECs.

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