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).

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.

In vitro release of vascular endothelial growth factor during platelet aggregation

1998 ◽  
Vol 275 (3) ◽  
pp. H1054-H1061 ◽  
Author(s):  
James P. Maloney ◽  
Christopher C. Silliman ◽  
Daniel R. Ambruso ◽  
Jun Wang ◽  
Rubin M. Tuder ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Platelet Aggregation ◽  
Growth Factor ◽  
Platelet Rich Plasma ◽  
In Vitro Release ◽  
Endothelial Permeability ◽  
Vascular Endothelial ◽  
Vessel Injury ◽  
Endothelial Growth Factor

Platelet aggregation is a cardinal feature of both vascular repair and vascular disease. During aggregation platelets release a variety of vasoactive substances; some of these promote angiogenesis, endothelial permeability, and endothelial growth, actions shared by vascular endothelial growth factor (VEGF). This study was undertaken to investigate the hypothesis that VEGF is released by aggregating platelets. We found that VEGF was secreted during the in vitro aggregation of platelet-rich plasma induced by thrombin, collagen, epinephrine, and ADP (range 23–518 pg VEGF/ml). Furthermore, serum VEGF levels were elevated compared with plasma (230 ± 63 vs. 38 ± 8 pg VEGF/ml), indicative of VEGF release during whole blood coagulation. Lysates of apheresed, leukocyte-poor platelet units contained significant amounts of VEGF (2.4 ± 0.8 pg VEGF/mg protein). VEGF message and protein were also present in a megakaryocytic cell line (Dami cell). These results suggest constitutive roles for platelet VEGF in the repair of intimal vessel injury and in the altered permeability and intimal proliferation seen at sites of platelet aggregation and thrombosis.

scholarly journals Assessment of Vascular Endothelial Growth Factor in Fresh versus Frozen Platelet Rich Plasma

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Nada Hosny ◽  
Fikry Goubran ◽  
Basma BadrEldin Hasan ◽  
Noha Kamel
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Calcium Gluconate ◽  
Platelet Rich Plasma ◽  
Vascular Endothelial ◽  
High Concentration ◽  
Significant Difference ◽  
Growth Factor Release ◽  
Endothelial Growth Factor ◽  
Vegf Release

Platelet rich plasma (PRP) is hemoconcentration with platelets concentration above baseline values and high concentration of many growth factors. The aim of this study was to assess freezing effect on vascular endothelial growth factor (VEGF) release from PRP using two different activation methods to simplify its use in different clinical applications. PRP was prepared using two-centrifugation steps method from 12 qualified blood donors. VEGF concentrations were measured in fresh PRP and after freezing/thawing for one and three weeks with two methods of activation using (i) calcium gluconate and (ii) calcium gluconate and thrombin. Platelets count was significantly increased compared to baseline whole blood values in all fresh and frozen PRP samples (p value was <0.05). No significant difference was found between VEGF concentrations after activating fresh and frozen-thawed PRP samples for one and three weeks by calcium alone or calcium with thrombin, and also no significant difference was found when freezing period was extended from one to three weeks. Our results showed that platelets count does not correlate with variable levels of VEGF. PRP could be prepared once and preserved frozen for at least three weeks for the next treatment sessions and activation with thrombin addition to calcium will not augment the growth factor release.

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