Baicalein potently suppresses angiogenesis induced by vascular endothelial growth factor through the p53/Rb signaling pathway leading to G1/S cell cycle arrest

2011 ◽  
Vol 236 (7) ◽  
pp. 851-858 ◽  
Author(s):  
Yun Ling ◽  
Yan Chen ◽  
Pu Chen ◽  
Hui Hui ◽  
Xiuming Song ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cell Cycle Arrest ◽  
Signaling Pathway ◽  
Vascular Endothelial ◽  
Cycle Arrest ◽  
Endothelial Growth Factor

scholarly journals Effect of luteolin on apoptosis and vascular endothelial growth factor in human choroidal melanoma cells

2021 ◽  
Vol 14 (2) ◽  
pp. 186-193
Author(s):  
Meng-Lin Shi ◽  
◽  
Hong-Fei Liao ◽  
Keyword(s):  
Cell Cycle ◽  
Flow Cytometry ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cell Cycle Arrest ◽  
Choroidal Melanoma ◽  
Vascular Endothelial ◽  
Cycle Arrest ◽  
Related Proteins ◽  
Endothelial Growth Factor

AIM: To investigate the effects of luteolin on apoptosis, the cell cycle, and the expression and secretion of vascular endothelial growth factor (VEGF) in human choroidal melanoma cells (C918 and OCM-1). METHODS: C918 and OCM-1 cells cultured in vitro were treated with various concentrations of luteolin (0, 5, 10, 15 μmol/L). Cell growth was observed with an inverted microscope, and cell cycle arrest was detected by propidium iodide (PI) staining using flow cytometry. Apoptosis was detected by Hoechst33342 staining, and apoptosis rate was determined by Annexin V-FITC/PI experiments using flow cytometry. The expression of apoptosis-related proteins Bcl-2, Bax and VEGF was analyzed using Western blots. The levels of VEGF secreted by the cells into the supernatant was analyzed using ELISA. RESULTS: After treating with 5 to 15 μmol/L luteolin for 48h, the fusion degree of C918 and OCM-1 cells decreased, and more floating apoptotic cells appeared. Luteolin treatment increased the G0-G1 phase ratio of the C918 and OCM-1 cells, blocked cell cycle progression, and increased the apoptosis rate of the C918 and OCM-1 cells. Western blot showed that luteolin decreased the expression of Bcl-2 and VEGF in the C918 and OCM-1 cells and increased the expression of Bax protein. The ELISA results showed that 10 to 15 μmol/L luteolin decreased the cell secretion of VEGF. CONCLUSION: Luteolin may induce apoptosis by regulating the levels of apoptosis-related proteins in C918 and OCM-1 cells. Luteolin can induce cell cycle arrest, decrease the expression of VEGF.

Knockdown of Nrf2 inhibits angiogenesis by downregulating VEGF expression through PI3K/Akt signaling pathway in cerebral microvascular endothelial cells under hypoxic conditions

2018 ◽  
Vol 96 (4) ◽  
pp. 475-482 ◽  
Author(s):  
Yujing Huang ◽  
Ying Mao ◽  
Huiying Li ◽  
Guangxun Shen ◽  
Guangxian Nan
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Ischemic Stroke ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Tube Formation ◽  
Vascular Endothelial ◽  
Akt Signaling Pathway ◽  
Microvascular Endothelial ◽  
Endothelial Growth Factor

Ischemic stroke is a major cerebrovascular disease resulting from a transient or permanent local reduction of cerebral blood flow. Angiogenesis plays an important role in cerebral microvascular repair after ischemic stroke. This study aimed at investigating the effect of NF-E2-related factor 2 (Nrf2) on the angiogenesis of mouse cerebral microvascular endothelial bEnd.3 cells in a hypoxic environment. We found that Nrf2 expression was temporarily increased in hypoxia-induced bEnd.3 cells. Knockdown of Nrf2 inhibited the proliferation, migration, as well as tube formation in hypoxia-induced bEnd.3 cells. Meanwhile, vascular endothelial growth factor and PI3K/Akt signaling pathways were identified to be regulated by Nrf2 in hypoxia-induced bEnd.3 cells. It was found that silencing of Nrf2 downregulated the expression levels of NAD(P)H:quinine oxidoreductase-1, vascular endothelial growth factor, p-Akt, and heme oxygenase-1 in hypoxia-induced bEnd.3 cells. Data suggested that hypoxia induced the transient increase of Nrf2, which plays a key role in the angiogenesis of cerebral microangiogenesis, and that Nrf2 regulates the proliferation, migration, as well as tube formation likely through PI3K/Akt signaling pathway in hypoxia-induced bEnd.3 cells. Our study provides proof of concept for the modulation of Nrf2, so as to tilt the balance toward angiogenesis, representing a therapeutic strategy for hypoxia or ischemia disorders such as stroke.

Stromal Vascular Fraction and Platelet-Rich Plasma Upregulate Vascular Endothelial Growth Factor Expression to Promote Hair Growth via the Wnt/β-Catenin Signaling Pathway

2019 ◽  
Vol 11 (12) ◽  
pp. 1685-1692
Author(s):  
Yarui Liu ◽  
Jindou Jiang ◽  
Yuan Ye ◽  
Zhehao Li ◽  
Meijun Tan ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Hair Follicle ◽  
Signaling Pathway ◽  
Hair Growth ◽  
Platelet Rich Plasma ◽  
Stromal Vascular Fraction ◽  
Follicle Cells ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Androgenetic alopecia (AGA) is a hair loss disease. At present, use of the stromal vascular fraction (SVF) and platelet-rich plasma (PRP) are thought to be the novel, safe, and effective treatment options of AGA, but the mechanism by which SVF and PRP promote hair growth is unclear. Here, we investigated the mechanism underlying the effects of SVF and PRP on hair growth by in vitro culture and in vivo modeling. SVF and PRP promoted hair growth, as was evident from the observation and counting of hair on the back skin of nude mice using ImageJ software. SVF and PRP promoted hair growth, and SVF worked better. We performed nucleic acid extraction with nanomagnetic beads, and the protein levels were extracted with a bicinchoninic acid protein assay kit. The results of western blot analysis and quantitative polymerase chain reaction (qPCR) showed that both SVF and PRP promoted the expression of anti-apoptotic genes. The effect of SVF was better than that of PRP. The results of EdU and hematoxylin and eosin staining showed that SVF and PRP induced the proliferation of hair follicle cells. SVF exerted better effects on the proliferation of hair follicle cells than PRP. Enzyme-linked immunosorbent assay (ELISA) results showed that the expression of the proteins associated with the Wnt/β-catenin process, including vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), alkaline phosphatase (ALP), Wnt10b, and β-catenin, significantly increased in the SVF-treated and PRP-treated dermal/epidermal cells as compared with the control cells. Therefore, SVF and PRP increased the expression of VEGF and PDGF through the Wnt/β-catenin signaling pathway to promote hair growth. The effect of SVF on dermal cells/epidermal cells was stronger than that of PRP, and the difference was statistically significant (P < 0.05).

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