Evaluation of Plasma Growth Factors (VEGF, PDGF, EGF, ANG1, and ANG2) in Patients with Varicose Veins Before and After Treatment with Endovenous Laser Ablation

Al-Zoubi, Nabil A; Yaghan, Rami J.; Mazahreh, Tagleb S.; Hijazi, Emad M.; Alqudah, Ahmad M.; Owaisy, Yasmin N; Hamouri, Shadi; Al-Shatnawi, Nawaf J.

doi:10.1089/pho.2017.4355

Cited by 4 publications

(4 citation statements)

References 15 publications

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“…The concentrations of VEGF, a proangiogenic cytokine which promotes neovascularisation and increases vascular permeability, were found to be lower in the CVD group. Similar observations were made in a study comparing cytokine concentrations before and after endovenous laser ablation, where VEGF was found in lower concentrations in the blood of the patients before surgery [37]. In other studies, however, the concentrations of VEGF were higher in CVD patients: both in the venous tissue [22] and in the peripheral blood [36, 38].…”

Section: Resultssupporting

confidence: 79%

Chemokines and Growth Factors Produced by Lymphocytes in the Incompetent Great Saphenous Vein

Grudzińska

Grzegorczyn

Czuba

2019

Mediators of Inflammation

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The role of cytokines in the pathogenesis of chronic venous disease (CVD) remains obscure. It has been postulated that oscillatory flow present in incompetent veins causes proinflammatory changes. Our earlier study confirmed this hypothesis. This study is aimed at assessing chemokines and growth factors (GFs) released by lymphocytes in patients with great saphenous vein (GSV) incompetence. In 34 patients exhibiting reflux in GSV, blood was derived from the cubital vein and from the incompetent saphenofemoral junction. In 12 healthy controls, blood was derived from the cubital vein. Lymphocyte culture with and without stimulation by phytohemagglutinin (PHA) was performed. Eotaxin, interleukin 8 (IL-8), macrophage inflammatory protein 1 A and 1B (MIP-1A and MIP-1B), interferon gamma-induced protein (IP-10), monocyte chemoattractant protein-1 (MCP-1), interleukin 5 (IL-5), fibroblast growth factor (FGF), granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF), platelet-derived growth factor-BB (PDGF-BB), and vascular endothelial growth factor (VEGF) were assessed in culture supernatants by a Bio-Plex assay. Higher concentrations of eotaxin and G-CSF were revealed in the incompetent GSV, compared with the concentrations in the patients' upper limbs. The concentrations of MIP-1A and MIP-1B were higher in the CVD group while the concentration of VEGF was lower. In the stimulated cultures, the concentration of G-CSF proved higher in the incompetent GSV, as compared with the patients' upper limbs. Between the groups, the concentration of eotaxin was higher in the CVD group, while the IL-5 and MCP-1 concentrations were lower. IL-8, IP-10, FGF, GM-CSF, and PDGF-BB did not reveal any significant differences in concentrations between the samples. These observations suggest that the concentrations of chemokines and GFs are different in the blood of CVD patients. The oscillatory flow present in incompetent veins may play a role in these changes. However, the role of cytokines in CVD requires further study.

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Section: Resultssupporting

confidence: 79%

Chemokines and Growth Factors Produced by Lymphocytes in the Incompetent Great Saphenous Vein

Grudzińska

Grzegorczyn

Czuba

2019

Mediators of Inflammation

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“…In patients with chronic venous disease, an elevated plasma levels of VEGF was revealed, which increased with disease severity 19 41. Some studies demonstrated altered plasma/serum concentration of VEGF among patients with varicose veins before and postoperative, and it may support its role in the pathogenesis of disease 42–44. However, the evaluation of studied factor in tissue is of particular importance, because VEGF plasma level does not reflect its role in the pathogenesis of the disease 18 41.…”

Section: Discussionmentioning

confidence: 99%

“…19 41 Some studies demonstrated altered plasma/ serum concentration of VEGF among patients with varicose veins before and postoperative, and it may support its role in the pathogenesis of disease. [42][43][44] However, the evaluation of studied factor in tissue is of particular importance, because VEGF plasma level does not reflect its role in the pathogenesis of the disease. 18 41 In the present study, we demonstrated increased VEGF-A content in varicose veins in comparison with the normal vein wall.…”

Section: Original Researchmentioning

confidence: 99%

Peptide growth factors and their receptors in the vein wall

Bruczko-Goralewska

Romanowicz

Bączyk

et al. 2019

Journal of Investigative Medicine

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The varicose vein wall remodeling is a very complex process, which is controlled by numerous factors, including peptide growth factors. The aim of the study was to assess a/b FGF, IGF-1, TGF-β1, VEGF-A and their receptors in the vein wall. Varicose vein samples were taken from 24 patients undergoing varicose vein surgery. The control material consisted of vein specimens collected from 12 patients with chronic limb ischemia. Contents of aFGF, bFGF, IGF-I, TGF-β1, VEGF, IGF-1R, VEGF R1 and VEGF R2 were assessed with ELISA method. Protein expression of FGF R1 and TGF-β RII were evaluated with western blot. Increased contents of aFGF, IGF-1 and VEGF-A were found in varicose veins in comparison with normal ones (p<0.05). In contrast, a significant decrease in TGF-β content was demonstrated in varicose veins (p<0.05). Furthermore, there was no difference in bFGF content in both groups (p>0.05). IGF-1 R content was significantly increased in varicose veins (p<0.05). There was no difference in VEGF R1 content between varicose and normal veins (p>0.05), whereas VEGF R2 content was significantly increased in varicose veins (p<0.05). Western blot demonstrated increased expression of TGF-β RII in varicose veins (p<0.05) and similar expression of FGF R1 in both groups (p>0.05). Demonstrated changes in peptide growth factors and their receptors may disturb metabolism of extracellular matrix in the varicose vein wall and contribute to the development of the disease to its more advanced stages.

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“…In addition, EGF has been indicated to contribute to the permeability of ECs and vascular tube formation, in particular, inducing endothelial cadherin tyrosine phosphorylation (6,13,60,68). Furthermore, both EGF and VEGF belong to the class of plasma growth factors; the expression of EGF and VEGF or their receptors is closely associated with atherosclerotic or other vascular diseases (2,47,72). It has also been reported that VEGF could upregulate the expression of EGF receptors (EGFRs); many inhibitors could block both EGFRs and VEGF receptors (VEGFRs), and there appears to be cross-talk between EGFR and VEGFR pathways (24,31,36,41,51,65).…”

Section: Introductionmentioning

confidence: 99%

Effect of melatonin on EGF- and VEGF-induced monolayer permeability of HUVECs

Yang

Zhang

et al. 2019

American Journal of Physiology-Heart and Circulatory Physiology

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Melatonin is a natural hormone involved in the regulation of circadian rhythm, immunity, and cardiovascular function. In the present study, we focused on the mechanism of melatonin in the regulation of vascular permeability. We found that melatonin could inhibit both VEGF- and EGF-induced monolayer permeability of human umbilical vein endothelial cells (HUVECs) and change the tyrosine phosphorylation of vascular-endothelial (VE-)cadherin, which was related to endothelial barrier function. In addition, phospho-AKT (Ser473) and phospho-ERK(1/2) played significant roles in the regulation of VE-cadherin phosphorylation. Both the phosphatidylinositol 3-kinase/AKT inhibitor LY49002 and MEK/ERK inhibitor U0126 could inhibit the permeability of HUVECs, but with different effects on tyrosine phosphorylation of VE-cadherin. Melatonin can influence the two growth factor-induced phosphorylation of AKT (Ser473) but not ERK(1/2). Our results show that melatonin can inhibit growth factor-induced monolayer permeability of HUVECs by influencing the phosphorylation of AKT and VE-cadherin. Melatonin can be a potential treatment for diseases associated with abnormal vascular permeability. NEW & NOTEWORTHY We found that melatonin could inhibit both EGF- and VEGF-induced monolayer permeability of human umbilical vein endothelial cells, which is related to phosphorylation of vascular-endothelial cadherin. Blockade of phosphatidylinositol 3-kinase/AKT and MEK/ERK pathways could inhibit the permeability of human umbilical vein endothelial cells, and phosphorylation of AKT (Ser473) might be a critical event in the changing of monolayer permeability and likely has cross-talk with the MEK/ERK pathway.

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Evaluation of Plasma Growth Factors (VEGF, PDGF, EGF, ANG1, and ANG2) in Patients with Varicose Veins Before and After Treatment with Endovenous Laser Ablation

Cited by 4 publications

References 15 publications

Chemokines and Growth Factors Produced by Lymphocytes in the Incompetent Great Saphenous Vein

Chemokines and Growth Factors Produced by Lymphocytes in the Incompetent Great Saphenous Vein

Peptide growth factors and their receptors in the vein wall

Effect of melatonin on EGF- and VEGF-induced monolayer permeability of HUVECs

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