scholarly journals Modulation of platelet-derived growth factor receptor expression in microvascular endothelial cells during in vitro angiogenesis.

1994 ◽  
Vol 93 (1) ◽  
pp. 131-139 ◽  
Author(s):  
M Marx ◽  
R A Perlmutter ◽  
J A Madri
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Growth Factor Receptor ◽  
Receptor Expression ◽  
Platelet Derived Growth Factor ◽  
Microvascular Endothelial Cells ◽  
Microvascular Endothelial ◽  
In Vitro Angiogenesis

Hydroxysafflor yellow A promotes angiogenesis in rat brain microvascular endothelial cells injured by oxygen-glucose deprivation/reoxygenation(OGD/R) through SIRT1-HIF-1α-VEGFA signaling pathway

2021 ◽  
Vol 18 ◽  
Author(s):  
Juxuan Ruan ◽  
Lei Wang ◽  
Jiheng Dai ◽  
Jing Li ◽  
Ning Wang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Ischemia Reperfusion ◽  
Tube Formation ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
Hydroxysafflor Yellow A ◽  
Microvascular Endothelial

Objective: Angiogenesis led by brain microvascular endothelial cells (BMECs) contributes to the remission of brain injury after brain ischemia reperfusion. In this study, we investigated the effects of hydroxysafflor yellow A(HSYA) on angiogenesis of BMECs injured by OGD/R via SIRT1-HIF-1α-VEGFA signaling pathway. Methods: The OGD/R model of BMECs was established in vitro by OGD for 2h and reoxygenation for 24h. At first, the concentrations of vascular endothelial growth factor (VEGF), Angiopoietin (ang) and platelet-derived growth factor (PDGF) in supernatant were detected by ELISA, and the proteins expression of VEGFA, Ang-2 and PDGFB in BMECs were tested by western blot; the proliferation, adhesion, migration (scratch healing and transwell) and tube formation experiment of BMECs; the expression of CD31 and CD34 were tested by immunofluorescence staining. The levels of sirtuin1(SIRT1), hypoxia-inducible factor-1α (HIF-1α), VEGFA mRNA and protein were tested. Results: HSYA up-regulated the levels of VEGF, Ang and PDGF in the supernatant of BMECs under OGD/R, and the protein expression of VEGFA, Ang-2 and PDGFB were increased; HSYA could significantly alleviate the decrease of cell proliferation, adhesion, migration and tube formation ability of BMECs during OGD/R; HSYA enhanced the fluorescence intensity of CD31 and CD34 of BMECs during OGD/R; HSYA remarkably up-regulated the expression of SIRT1, HIF-1α, VEGFA mRNA and protein after OGD/R, and these increase decreased after SIRT1 was inhibited. Conclusion: SIRT1-HIF-1α-VEGFA signaling pathway is involved in HSYA improves angiogenesis of BMECs injured by OGD/R.

scholarly journals Gui Shao Di Huang Wan promotes angiogenesis and regulates oestrogen receptor α and progesterone receptor β in in vitro bioassays

2021 ◽  
Author(s):  
Rebecca O'Cleirigh ◽  
Rozlyn Gibbs
Keyword(s):  
Endothelial Cells ◽  
Progesterone Receptor ◽  
Mtt Assay ◽  
Receptor Expression ◽  
Microvascular Endothelial Cells ◽  
Ishikawa Cells ◽  
In Vitro Bioassays ◽  
Microvascular Endothelial ◽  
Er Alpha

Background and aim: The formula Gui Shao Di Huang Wan (GSDW) is used frequently to treat female infertility. This study aims to investigate some of the possible mechanisms of action of GSDW using in vitro bioassays of angiogenesis in Human Uterine Microvascular Endothelial Cells (HUVEC) and Human Uterine Microvascular Endothelial Cells (HUtMEC) and ovarian steroid receptor expression in a human endometrial cell line (Ishikawa). Experimental procedure: Aqueous extracts of GSDW and its component herbs were tested for pro-angiogenic activity using both HUVEC and HUtMEC 2D differentiation assays performed on Matrigel and effects on HUVEC proliferation using the MTT assay. Effects on the expression of Estrogen Receptor alpha (ER alpha) and Progesterone Receptor beta (PRbeta) in Ishikawa cells were determined using immunoblotting. Results and Conclusion: ll analysed parameters of differentiation were increased by GSDW in both the HUVEC and HUtMEC mesh. Furthermore, measures of total length, segment number, junction number were affected by some but not all component herbs. The MTT assay showed an increase in proliferation of HUVECs at concentrations of GSDW between 0.68 and 5.47 ug/mL at 48 and 72 hours. In Ishikawa cells downregulation of ER alpha; and upregulation of PR beta; was seen after 48 hours incubation with 4 of the 8 herbs in the formula. The findings in this study demonstrate that GSDW has the potential to affect key parameters (vascular, sex hormone receptor expression) in vitro. This offers a mechanism by which these herbs may enhance fertility through improved endometrial receptivity and pregnancy rates.

Hypoxia in combination with FGF-2 induces tube formation by human microvascular endothelial cells in a fibrin matrix: involvement of at least two signal transduction pathways

2001 ◽  
Vol 114 (4) ◽  
pp. 825-833 ◽  
Author(s):  
M.E. Kroon ◽  
P. Koolwijk ◽  
B. van der Vecht ◽  
V.W. van Hinsbergh
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Tube Formation ◽  
Microvascular Endothelial Cells ◽  
Signal Pathways ◽  
Fibrin Matrix ◽  
Hypoxic Conditions ◽  
Mitogen Activated Protein ◽  
Microvascular Endothelial

Hypoxia in combination with a growth factor is a strong inducer of angiogenesis. Among several effects, hypoxia can activate endothelial cells directly, but the mechanism by which it acts is not fully elucidated. In vitro, human microvascular endothelial cells (hMVEC) form capillary-like tubules in fibrin solely after stimulation with a combination of fibroblast growth factor (FGF)-2 or vascular endothelial growth factor (VEGF) and the cytokine tumour necrosis factor (TNF)alpha. We show in this paper that in hypoxic conditions, FGF-2-stimulated hMVEC form tube-like structures in a fibrin matrix in the absence of TNFalpha. Hypoxia/FGF-2-stimulated cells express more urokinase-type plasminogen activator (u-PA) receptor than normoxia/FGF-2-stimulated cells and display a slightly higher turnover of u-PA. This small increase in u-PA activation probably cannot fully explain the hypoxia/FGF-2-induced tube formation. Hypoxia activated at least two signal pathways that may contribute to the enhanced angiogenic response. In hypoxia/FGF-2-stimulated hMVEC the transcription factor p65 was activated and translocated to the nucleus, whereas in normoxia/FGF-2-stimulated cells p65 remained inactive. Furthermore, in hypoxic conditions, the amounts of phosphorylated mitogen-activated protein kinases ERK1/2 were increased compared to normoxic conditions. We conclude that hypoxia is able to activate different signal pathways in FGF-2-stimulated human endothelial cells, which may be involved in hypoxia-induced angiogenesis.

PAX2 expression by HHV-8–infected endothelial cells induced a proangiogenic and proinvasive phenotype

Blood ◽  
2008 ◽  
Vol 111 (5) ◽  
pp. 2806-2815 ◽  
Author(s):  
Valentina Fonsato ◽  
Stefano Buttiglieri ◽  
Maria Chiara Deregibus ◽  
Benedetta Bussolati ◽  
Elisabetta Caselli ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Scid Mice ◽  
Microvascular Endothelial Cells ◽  
Stable Transfection ◽  
Microvascular Endothelial ◽  
In Vitro Angiogenesis ◽  
Pax2 Gene ◽  
Pax2 Expression

In the present study, we evaluated whether infection of microvascular endothelial cells (HMECs) with HHV-8 can trigger the expression of PAX2 oncogene and whether PAX2 protein is involved in HHV-8–induced transformation of HMECs. We found that HHV-8 infection induced the expression of both the PAX2 gene and PAX2 protein in HMECs but failed to induce PAX2 protein in HMECs stably transfected with PAX2 antisense (HMEC-AS). HHV-8–infected HMECs but not HMEC-AS acquired proinvasive proadhesive properties, enhanced survival and in vitro angiogenesis, suggesting a correlation between PAX2 expression and the effects triggered by HHV-8 infection. When HMEC-expressing PAX2 by stable transfection with PAX2 sense gene or by HHV-8 infection were implanted in vivo in severe combined immunodeficient (SCID) mice, enhanced angiogenesis and proliferative lesions resembling KS were observed. HHV-8–infected HMEC-AS failed to induce angiogenesis and KS-like lesions. These results suggest that the expression of PAX2 is required for the proangiogenic and proinvasive changes induced by HHV-8 infection in HMECs. In conclusion, HHV-8 infection may activate an embryonic angiogenic program in HMECs by inducing the expression of PAX2 oncogene.

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