Effects of Hypocrellin A on Expression of Vascular Endothelial Growth Factor and Endothelin-1 in Human Umbilical Endothelial Cells

2007 ◽  
Vol 35 (04) ◽  
pp. 713-723 ◽  
Author(s):  
Lei Dang ◽  
J. Paul Seale ◽  
Xianqin Qu
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Endothelial Dysfunction ◽  
Protein Expression ◽  
Vascular Endothelial ◽  
Naturally Occurring ◽  
Hypocrellin A ◽  
Endothelial Growth Factor ◽  
Vegf Protein

Increased endothelin-1 (ET-1), vascular endothelial growth factor (VEGF) and activation of protein kinase C (PKC) are co-contributors to endothelial hyperpermeability in diabetes. Several lines of evidence have suggested a hypothesis that activation of specific PKC isoforms are the causative factor in ET-1 and VEGF mediated endothelial dysfunction. In the present study, we tested this hypothesis with hypocrellin A, a naturally occurring PKC inhibitor from a Chinese plant. Human umbilical vein endothelial cells (HUVECs) were incubated with 20 mM glucose in both the presence and absence of hypocrellin A, after which, the protein expression and release of VEGF and mRNA expression and release of ET-1 were measured. VEGF and ET-1 were released into the medium and expressions of VEGF protein and ET-1 mRNA were significantly increased in HUVECs incubated with 20 mM glucose. Hypocrellin A (150 nM) significantly decreased VEGF release (117 ± 3 vs. 180 ± 11 pg/mg, p < 0.05) and VEGF protein expression (from 130 ± 14% to 88 ± 18.5%, p < 0.05). ET-1 release was also reduced in hypocrellin A treated HUVECs (63.3 ± 9.9 vs. 75.2 ± 12.6 ng/mg). Hypocrellin A significantly reversed the effect of high glucose on ET-1 mRNA expression ( p < 0.05). The results revealed that PKC activation plays a pivotal role in VEGF and ET-1 mediated endothelial permeability. The naturally occurring compound hypocrellin A may be a potentially novel treatment for endothelial dysfunction in diabetes.

scholarly journals Nitric oxide mediates the mitogenic effects of insulin and vascular endothelial growth factor but not of leptin in endothelial cells.

1999 ◽  
Vol 46 (3) ◽  
pp. 703-715 ◽  
Author(s):  
A Józkowicz ◽  
J Pankiewicz ◽  
J Dulak ◽  
L Partyka ◽  
I Wybrańska ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor ◽  
Vegf Protein

The regulation of vascular wall homeostasis by nitric oxide (NO) generated by endothelium is being intensively studied. In the present paper, the involvement of NO in the vascular endothelial growth factor (VEGF), insulin or leptin-stimulated proliferation of human endothelial cells (HUVEC) was measured by [3H]thymidine or bromodeoxyuridine incorporation. VEGF and insulin, but not leptin, increased NO generation in HUVEC, as detected with ISO-NO electrode. Proliferation of HUVEC induced by leptin was not changed or was higher in the presence of N(omega)-nitro-L-arginine methyl ester (L-NAME) a nitric oxide synthase (NOS) inhibitor. In contrast, L-NAME blunted the proproliferative effect of VEGF and insulin. Furthermore, we demonstrated that, in human arterial smooth muscle cells (hASMC) transfected with endothelial NOS (eNOS) gene, the generation of biologically active VEGF protein was NO-dependent. Inhibition of NO generation by L-NAME decreased the synthesis of VEGF protein and attenuated HUVEC proliferation induced by conditioned media from transfected hASMC. Endothelium-derived NO seems to participate in VEGF and insulin, but not leptin, mitogenic activity. Additionally, the small amounts of NO released from endothelial cells, as mimicked by eNOS transfection into hASMC, may activate generation of VEGF in sub-endothelial smooth muscle cells, leading to increased synthesis of VEGF protein necessary for turnover and restitution of endothelial cells.

Expression of Vascular Endothelial Growth Factor in Human Umbilical Vein Endothelial Cells Stimulated with Interleukin-1α

2000 ◽  
Vol 83 (06) ◽  
pp. 949-955 ◽  
Author(s):  
Hiroyuki Itaya ◽  
Satoki Nasu ◽  
Hidemi Yoshida ◽  
Yuki Matsubara ◽  
Koji Fujimoto ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Umbilical Vein ◽  
Vascular Endothelial ◽  
Vegf Mrna ◽  
Interleukin 1Α ◽  
Umbilical Vein Endothelial Cells ◽  
Endothelial Growth Factor ◽  
Vegf Protein

SummaryVascular endothelial growth factor (VEGF) is a specific mitogen for endothelial cells. We studied the production of VEGF by human umbilical vein endothelial cells (HUVEC) and smooth muscle cells (SMC) in response to the stimulation with interleukin-1α (IL-1α). HUVEC expressed VEGF mRNA in response to IL-1α in doseand time-dependent manners. In HUVEC VEGF protein was detected only in cell lysates whereas in SMC most of the VEGF protein was detected in the conditioned medium. Immunofluorescent staining also confirmed the cell-associated VEGF in HUVEC. IL-1α also induced the expression of mRNA for IL-1α itself in HUVEC. Cycloheximide treatment of HUVEC slightly inhibited the IL-1α-induced expression of VEGF mRNA, and IL-1α may mediate, at least in part, VEGF expression in response to IL-1α. The growth of HUVEC stimulated with IL-1α was inhibited by a neutralizing antibody against VEGF. We conclude that IL-1α and VEGF may play an important role in autocrine growth regulation of HUVEC.

scholarly journals Effect of ovarian steroids on vascular endothelial growth factor a expression in bovine uterine endothelial cells during adenomyosis

2019 ◽  
Vol 15 (1) ◽  
Author(s):  
Martyna Lupicka ◽  
Anna Zadroga ◽  
Agata Szczepańska ◽  
Anna Justyna Korzekwa
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Protein Expression ◽  
Vascular Endothelial Cells ◽  
Quantitative Polymerase Chain Reaction ◽  
Vascular Endothelial ◽  
Gene And Protein Expression ◽  
Endothelial Growth Factor

Abstract Background Adenomyosis is a uterine dysfunction defined as the presence of endometrial glands within the myometrium. There is evidence that proangiogenic factors may play a role during the development of adenomyosis; however, exact mechanism remains unknown. The aim of the study was to determine the action of vascular endothelial growth factor A (VEGFA) in uterine tissue and uterine vascular endothelial cells during adenomyosis. Results Uterine tissues were collected and examined for the presence and extent of adenomyosis. Gene and protein expression of VEGFA and its two receptors (VEGFR1 and VEGFR2) was evaluated with quantitative polymerase chain reaction and Western blotting, respectively, in endometrium and myometrium during adenomyosis. Immunolocalization of VEGFA and its receptors within uterine tissues during adenomyosis was also determined. In an in vitro experiment, endothelial cells from non-adenomyotic bovine uteri were treated with media conditioned by non-adenomyotic or adenomyotic uterine slices treated with 17-beta-oestradiol (E2) or progesterone (P4). Both gene and protein expression of VEGFR2 were elevated in endometrium in stages 3–4 of adenomyosis. Protein expression of VEGFA and VEGFR2 as well as VEGFA secretion were increased in endothelial cells treated with media conditioned by adenomyotic uterine slices after E2 treatment. Conclusions Results suggest that VEGFA signalling is an important component, next to E2, that enhances VEGFA action and participates in adenomyosis development in cows.

scholarly journals Diagnostic and prognostic value of endothelial dysfunction markers in patients with ulcerative colitis

2016 ◽  
Vol 97 (2) ◽  
pp. 187-191 ◽  
Author(s):  
E A Stepina ◽  
O V Khlynova ◽  
A V Tuev
Keyword(s):  
Ulcerative Colitis ◽  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Endothelial Dysfunction ◽  
Pathological Process ◽  
Control Group ◽  
Vascular Endothelial ◽  
Disease Attack ◽  
Endothelial Growth Factor

Aim. To assess the endothelial dysfunction degree in patients with ulcerative colitis, depending on the disease attack severity, the pathological process spread, the presence of systemic manifestations, complications, and endoscopic activity of the process.Methods. 45 patients with an established diagnosis of «ulcerative colitis» in the exacerbation phase and with newly diagnosed disease forms were examined. The control group included 11 apparently healthy people. As endothelial dysfunction markers vascular endothelial growth factor levels in serum and blood plasma desquamated endothelial cells amount were studied.Results.In the group of patients with ulcerative colitis a statistically significant increase in levels of endothelial dysfunction markers (the vascular endothelial growth factor content was 506.40±287.00 pg/ml, the plasma desquamated endothelial cells number - 6.47±4.22×104/L) was found compared with the control group (pConclusion. In patients with ulcerative colitis endothelial dysfunction, correlated with disease activity and severity markers, was revealed; vascular endothelial growth factor levels and plasma desquamated endothelial cells number can serve as the ulcerative colitis severity criteria, as well as a sign of unfavorable disease course.

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