Increase of Vascular Endothelial Growth Factor and Decrease of MCP-1 and Some Updated Epidemiology Aspects of Cystic Echinococcosis Human Cases in Calabria Region

We aim to investigate some of the pathogenetic mediators of the human echinococcosis and to obtain updated epidemiological findings on cases of echinococcosis in Calabria, Southern Italy. Echinococcosis diagnosis was based on imaging, serological investigations, and molecular assay. Indeed, real-time PCR indicated the presence of G2/G3 genotypes ofEchinococcus granulosuscomplex. Regarding pathogenesis, a relevant novel tool of immune depression should be deemed the reduced level of serum MCP-1. Also, we found a previously unreported VEGF, possibly associated with neovascularization requested by the parasite cyst metabolism. Cytokine profiles suggest a bias of the immunity toward Th2 and Treg responses. Nitric oxide levels exhibited a significant decrease one week after therapy versus basal level measured before surgery and/or chemotherapy. An increase of serum total IgE class and IgG4 subclass was found inEchinococcus-positive patients versus controls. Our data demonstrated an endemic spreading, at least in the province of Catanzaro and neighboring Calabria territories, for such parasitosis with the novel issue of the number of female overcoming male cases. In conclusion, the novel findings of this study were the increased VEGF and the reduced serum MCP-1 in the studied cases, as well as the number ofEchinococcus-infected females overcoming the infected males.

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Faculty Opinions recommendation of Ligand-independent activation of vascular endothelial growth factor receptor 2 by fluid shear stress regulates activation of endothelial nitric oxide synthase.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.13409087.14780102 ◽

2011 ◽

Author(s):

Martin A Schwartz

Keyword(s):

Nitric Oxide ◽

Vascular Endothelial Growth Factor ◽

Endothelial Nitric Oxide Synthase ◽

Fluid Shear Stress ◽

Growth Factor Receptor ◽

Vascular Endothelial ◽

Fluid Shear ◽

Oxide Synthase ◽

Endothelial Growth Factor ◽

Endothelial Nitric Oxide

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Pro-Angiogenic Effects of Resveratrol in Brain Endothelial Cells: Nitric Oxide-Mediated Regulation of Vascular Endothelial Growth Factor and Metalloproteinases

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.2012.2 ◽

2012 ◽

Vol 32 (5) ◽

pp. 884-895 ◽

Cited By ~ 43

Author(s):

Fabricio Simão ◽

Aline S Pagnussat ◽

Ji Hae Seo ◽

Deepti Navaratna ◽

Wendy Leung ◽

...

Keyword(s):

Nitric Oxide ◽

Vascular Endothelial Growth Factor ◽

Endothelial Cells ◽

Growth Factor ◽

Signaling Pathways ◽

Tube Formation ◽

Mitogen Activated Protein Kinase ◽

Vascular Endothelial ◽

Cerebral Endothelial Cells ◽

Endothelial Growth Factor

Resveratrol may be a powerful way of protecting the brain against a wide variety of stress and injury. Recently, it has been proposed that resveratrol not only reduces brain injury but also promotes recovery after stroke. But the underlying mechanisms are unclear. Here, we tested the hypothesis that resveratrol promotes angiogenesis in cerebral endothelial cells and dissected the signaling pathways involved. Treatment of cerebral endothelial cells with resveratrol promoted proliferation, migration, and tube formation in Matrigel assays. Consistent with these pro-angiogenic responses, resveratrol altered endothelial morphology resulting in cytoskeletal rearrangements of β-catenin and VE-cadherin. These effects of resveratrol were accompanied by activation of phosphoinositide 3 kinase (PI3-K)/Akt and Mitogen-Activated Protein Kinase (MAPK)/ERK signaling pathways that led to endothelial nitric oxide synthase upregulation and increased nitric oxide (NO) levels. Subsequently, elevated NO signaling increased vascular endothelial growth factor and matrix metalloproteinase levels. Sequential blockade of these signaling steps prevented resveratrol-induced angiogenesis in cerebral endothelial cells. These findings provide a mechanistic basis for the potential use of resveratrol as a candidate therapy to promote angiogenesis and neurovascular recovery after stroke.

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Predominant role of endothelial nitric oxide synthase in vascular endothelial growth factor-induced angiogenesis and vascular permeability

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.041359198 ◽

2001 ◽

Vol 98 (5) ◽

pp. 2604-2609 ◽

Cited By ~ 659

Author(s):

D. Fukumura ◽

T. Gohongi ◽

A. Kadambi ◽

Y. Izumi ◽

J. Ang ◽

...

Keyword(s):

Nitric Oxide ◽

Vascular Endothelial Growth Factor ◽

Growth Factor ◽

Endothelial Nitric Oxide Synthase ◽

Vascular Endothelial ◽

Predominant Role ◽

Oxide Synthase ◽

Endothelial Growth Factor ◽

Endothelial Nitric Oxide

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Inducible Nitric Oxide Synthase Mediates Hypoxia-Induced Hypoxia-Inducible Factor-1α Activation and Vascular Endothelial Growth Factor Expression in Oxygen-Induced Retinopathy

Pathobiology ◽

10.1159/000110027 ◽

2007 ◽

Vol 74 (6) ◽

pp. 336-343 ◽

Cited By ~ 17

Author(s):

Tao He ◽

Ming Ai ◽

Xiao-Hui Zhao ◽

Yi-Qiao Xing

Keyword(s):

Nitric Oxide ◽

Vascular Endothelial Growth Factor ◽

Hypoxia Inducible Factor ◽

Vascular Endothelial ◽

Oxygen Induced Retinopathy ◽

Factor Expression ◽

Growth Factor Expression ◽

Oxide Synthase ◽

Endothelial Growth Factor ◽

Inducible Nitric Oxide

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Induction of vascular endothelial growth factor by nitric oxide in cultured human articular chondrocytes

Biochimie ◽

10.1016/s0300-9084(01)01280-9 ◽

2001 ◽

Vol 83 (6) ◽

pp. 515-522 ◽

Cited By ~ 9

Author(s):

Kyril Turpaev ◽

Dmitry Litvinov ◽

Vera Dubovaya ◽

Andrey Panasyuk ◽

Dmitry Ivanov ◽

...

Keyword(s):

Nitric Oxide ◽

Vascular Endothelial Growth Factor ◽

Growth Factor ◽

Articular Chondrocytes ◽

Human Articular Chondrocytes ◽

Vascular Endothelial ◽

Endothelial Growth Factor

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Induction of Nitric Oxide Synthase (NOS) and Vascular Endothelial Growth Factor (VEGF) in Experimental Model of Angioplasty and Heart Ischemia

Advances in Experimental Medicine and Biology - Recent Advances in Prostaglandin, Thromboxane, and Leukotriene Research ◽

10.1007/978-1-4899-1810-9_33 ◽

1997 ◽

pp. 163-167 ◽

Cited By ~ 7

Author(s):

Aldona Dembinska-Kiec ◽

Jozef Dulak ◽

Lukasz Partyka ◽

Robert Krzesz ◽

Dariusz Dudek ◽

...

Keyword(s):

Nitric Oxide ◽

Vascular Endothelial Growth Factor ◽

Growth Factor ◽

Nitric Oxide Synthase ◽

Experimental Model ◽

Vascular Endothelial ◽

Heart Ischemia ◽

Oxide Synthase ◽

Endothelial Growth Factor

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AGE-RELATED CHANGES IN PROSTAGLANDIN E2, NITRIC OXIDE, AND VASCULAR ENDOTHELIAL GROWTH FACTOR LEVELS IN GASTRIC MUCOSA DURING THE HEALING OF ACETIC ACID-INDUCED ULCER

Asian Journal of Pharmaceutical and Clinical Research ◽

10.22159/ajpcr.2018.v11i10.28494 ◽

2018 ◽

Vol 11 (10) ◽

pp. 517

Author(s):

Ayodeji Folorunsho Ajayi ◽

Busuyi David Kehinde ◽

Olubodun Micheal Lateef ◽

Bolaji Aderibigbe Akorede

Keyword(s):

Nitric Oxide ◽

Vascular Endothelial Growth Factor ◽

Acetic Acid ◽

Growth Factor ◽

Gastric Mucosa ◽

Prostaglandin E2 ◽

Ulcer Healing ◽

Vascular Endothelial ◽

Epithelial Restitution ◽

Endothelial Growth Factor

Objective: Nitric oxide (NO), prostaglandin E2 (PgE2), and vascular endothelial growth factor (VEGF) are fundamental regulators of epithelial restitution and angiogenesis. They play important roles in ulcer healing. Insights into their possible changes during gastric ulcer healing putting age into consideration could give a guide to the proper management of ulcers in the aging population. This study, therefore, examined alterations in the concentrations of PgE2, NO, and VEGF in the gastric mucosa of rats of different ages after induction of ulcer and during healing.Methods: Male Wister rats (aged 3, 6, and 18 months old) were divided into three groups according to their ages. The ulcer was induced using the acetic acid ulcer model. Healing indices studied on days 3, 7, and 14 were the macroscopic dimension of ulcer, stomach tissue concentration of PgE2, NO, and VEGF, with the immunohistochemical expression of VEGF.Results: Outcome of this study showed 100%, 88.36%, and 62.30% area of mucosa healed in 3-, 6-, and 18-month-old rats respectively, on day 14 post-induction of ulcer. PgE2, NO, and VEGF concentrations were inversely proportional to age during healing. Immunohistochemical staining showed that younger rat (3 and 6 months old) had higher expression of VEGF throughout the healing period.Conclusion: It was therefore concluded that the slower rate of healing in older rats could be due to reduced gastroprotection, epithelial restitution, and angiogenesis as age increases.

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