scholarly journals Elevated levels of endothelial molecules ICAM-1, VEGF-A and VEGFR2 in microscopic asymptomatic malaria

2021 ◽  
Author(s):  
Augustina Frimpong ◽  
Jones Amponsah ◽  
Dorothy Agyemang ◽  
Abigail Sena Adjokatseh ◽  
Sophia Eyiah-Ampah ◽  
...  
Keyword(s):  
Operating Characteristic ◽  
Malaria Diagnosis ◽  
Endothelial Activation ◽  
Asymptomatic Malaria ◽  
Vascular Endothelial ◽  
Angiogenic Growth Factors ◽  
Characteristic Analysis ◽  
Asymptomatic Parasitaemia ◽  
Intracellular Adhesion Molecule ◽  
Endothelial Growth Factor

Abstract Background In malaria, clinical disease has been associated with increased levels of endothelial activation due to the sequestration of infected erythrocytes. However, levels and impact of endothelial activation and pro-angiogenic molecules such as vascular endothelial growth factor (VEGF)-A and its receptor VEGFR2 in asymptomatic malaria have not been well characterized. Methods Blood samples were obtained from community children for malaria diagnosis using microscopy and PCR. A multiplex immunoassay was used to determine the levels of Intracellular adhesion molecule (ICAM)-1, VEGF-A, and VEGFR2 in the plasma of children with microscopic or submicroscopic asymptomatic parasitaemia and compared with levels in uninfected controls. Results Levels of ICAM-1, VEGF-A and VEGFR2 were significantly increased in children with microscopic asymptomatic parasitaemia compared with uninfected controls. Also, levels of VEGF-A were found to be inversely associated with age. Additionally, a receiver operating characteristic analysis revealed that plasma levels of ICAM-1 (AUC =0.72), showed a moderate potential in discriminating between children with microscopic malaria from uninfected controls when compared to VEGF-A (AUC =0.67) and VEGFR2 (AUC =0.69). Conclusion These data imply that endothelial activation and pro-angiogenic growth factors could be one of the early host responders during microscopic asymptomatic malaria, and may play a significant role in disease pathogenesis.

scholarly journals Large adipose tissue generation in a mussel-inspired bioreactor of elastic–mimetic cryogel and platelets

2018 ◽  
Vol 9 ◽  
pp. 204173141880863 ◽  
Author(s):  
Qiang Chang ◽  
Junrong Cai ◽  
Ying Wang ◽  
Ruijia Yang ◽  
Malcolm Xing ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Adipose Tissue ◽  
Growth Factor ◽  
Cellular Proliferation ◽  
Platelet Derived Growth Factor ◽  
Control Group ◽  
Vascular Endothelial ◽  
Angiogenic Growth Factors ◽  
Congenital Deformities ◽  
Endothelial Growth Factor

Soft tissue generation, especially in large tissue, is a major challenge in reconstructive surgery to treat congenital deformities, posttraumatic repair, and cancer rehabilitation. The concern is along with the donor site morbidity, donor tissue shortage, and flap necrosis. Here, we report a dissection-free adipose tissue chamber–based novel guided adipose tissue regeneration strategy in a bioreactor of elastic gelatin cryogel and polydopamine-assisted platelet immobilization intended to improve angiogenesis and generate large adipose tissue in situ. In order to have matched tissue mechanics, we used 5% gelatin cryogel as growth substrate of bioreactor. Platelets from the platelet-rich plasma were then immobilized onto the gelatin cryogel with the aid of polydopamine to form a biomimetic bioreactor (polydopamine/gelatin cryogel/platelet). Platelets on the substrate led to a sustained high release in both platelet-derived growth factor and vascular endothelial growth factor compared with non-polydopamine-assisted group. The formed bioreactor was then transferred to a tissue engineering chamber and then inserted above inguinal fat pad of rats without flap dissection. This integrate strategy significantly boomed the vessel density, stimulated cellular proliferation, and upregulated macrophage infiltration. There was a noticeable rise in the expression of dual-angiogenic growth factors (platelet-derived growth factor and vascular endothelial growth factor) in chamber fluid; host cell migration and host fibrous protein secretion coordinated with gelatin cryogel degradation. The regenerated adipose tissue volume gained threefold larger than control group (p < 0.05) with less fibrosis tissue. These results indicate that a big well-vascularized three-dimensional mature adipose tissue can be regenerated using elastic gel, polydopamine, platelets, and small fat tissue.

scholarly journals Angiogenesis of endocrine gland tumours--new molecular targets in diagnostics and therapy

2002 ◽  
pp. 143-151 ◽  
Author(s):  
HM Stepien ◽  
K Kolomecki ◽  
Z Pasieka ◽  
J Komorowski ◽  
T Stepien ◽  
...  
Keyword(s):  
Growth Factor ◽  
Adhesion Molecule ◽  
Malignant Tumour ◽  
Cellular Adhesion ◽  
Endocrine Gland ◽  
Vascular Endothelial ◽  
Intracellular Adhesion Molecule ◽  
Cellular Adhesion Molecule ◽  
Adhesive Molecules ◽  
Endothelial Growth Factor

Angiogenesis is one of the key stages in the development of neoplastic tumours, in which a small group of mutated cells transforms into a large malignant tumour metastasising to the neighbouring tissues and organs. The studies on the significance of neoangiogenesis in the progression of endocrine gland neoplasms have recently become one of the most rapidly evolving branches of molecular endocrinology. The induction of angiogenesis has been demonstrated to result from the imbalance between positive and negative factors which control this process. Our paper presents the results of current studies on the role of factors such as molecular markers of angiogenesis (e.g. vascular endothelial growth factor and basic fibroblast growth factor), metalloproteinases (which regulate the decomposition of the extracellular matrix) and their inhibitors, and adhesive molecules (e.g. soluble vascular cellular adhesion molecule-1 and soluble intracellular adhesion molecule-1) in the pathogenesis and diagnostics of endocrine gland tumours in humans. Also, we discuss new therapeutic strategies for inhibiting the growth of neoplasms by blocking the formation of blood vessels using angiogenesis antagonists, which inhibit various stages of angiogenesis. More and more data are being accumulated suggesting that these preparations could, in the near future, be used in the pharmacotherapy of some endocrine gland neoplasms.

scholarly journals Binding affinities of vascular endothelial growth factor (VEGF) for heparin-derived oligosaccharides

2011 ◽  
Vol 32 (1) ◽  
pp. 71-81 ◽  
Author(s):  
Wenjing Zhao ◽  
Scott A. McCallum ◽  
Zhongping Xiao ◽  
Fuming Zhang ◽  
Robert J. Linhardt
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Binding Affinity ◽  
Structural Features ◽  
Minimum Size ◽  
Vascular Endothelial ◽  
Binding Affinities ◽  
Angiogenic Growth Factors ◽  
Protein Ligands ◽  
Endothelial Growth Factor

Heparin and HS (heparan sulfate) exert their wide range of biological activities by interacting with extracellular protein ligands. Among these important protein ligands are various angiogenic growth factors and cytokines. HS binding to VEGF (vascular endothelial growth factor) regulates multiple aspects of vascular development and function through its specific interaction with HS. Many studies have focused on HS-derived or HS-mimicking structures for the characterization of VEGF165 interaction with HS. Using a heparinase 1-prepared small library of heparin-derived oligosaccharides ranging from hexasaccharide to octadecasaccharide, we systematically investigated the heparin-specific structural features required for VEGF binding. We report the apparent affinities for the association between the heparin-derived oligosaccharides with both VEGF165 and VEGF55, a peptide construct encompassing exclusively the heparin-binding domain of VEGF165. An octasaccharide was the minimum size of oligosaccharide within the library to efficiently bind to both forms of VEGF and a tetradecasaccharide displayed an effective binding affinity to VEGF165 comparable to unfractionated heparin. The range of relative apparent binding affinities among VEGF and the panel of heparin-derived oligosaccharides demonstrate that the VEGF binding affinity likely depends on the specific structural features of these oligosaccharides, including their degree of sulfation, sugar-ring stereochemistry and conformation. Notably, the unique 3-O-sulfo group found within the specific antithrombin binding site of heparin is not required for VEGF165 binding. These findings afford new insight into the inherent kinetics and affinities for VEGF association with heparin and heparin-derived oligosaccharides with key residue-specific modifications and may potentially benefit the future design of oligosaccharide-based anti-angiogenesis drugs.

scholarly journals An unexpected tail of VEGF and PlGF in pre-eclampsia

2011 ◽  
Vol 39 (6) ◽  
pp. 1576-1582 ◽  
Author(s):  
David O. Bates
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Endothelial Activation ◽  
Placental Growth Factor ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Physiological Changes ◽  
Vegf Family Members ◽  
Endothelial Growth Factor ◽  
Vegf Isoforms

PET (pre-eclamptic toxaemia), characterized by pregnancy-related hypertension and proteinuria, due to widespread endothelial dysfunction, is a primary cause of maternal morbidity. Altered circulating factors, particularly the VEGF (vascular endothelial growth factor) family of proteins and their receptors, are thought to be key contributors to this disease. Plasma from patients with PET induces numerous cellular and physiological changes in endothelial cells, indicating the presence of a circulating imbalance of the normal plasma constituents. These have been narrowed down to macromolecules of the VEGF family of proteins and receptors. It has been shown that responses of endothelial cells in intact vessels to plasma from patients with pre-eclampsia is VEGF-dependent. It has recently been shown that this may be specific to the VEGF165b isoform, and blocked by addition of recombinant human PlGF (placental growth factor). Taken together with results that show that sVEGFR1 (soluble VEGF receptor 1) levels are insufficient to bind VEGF-A in human plasma from patients with pre-eclampsia, and that other circulating macromolecules bind, but do not inactivate, VEGF-A, this suggests that novel hypotheses involving altered bioavailability of VEGF isoforms resulting from reduced or bound PlGF, or increased sVEGFR1 increasing biological activity of circulating plasma, could be tested. This suggests that knowing how to alter the balance of VEGF family members could prevent endothelial activation, and potentially some symptoms, of pre-eclampsia.

scholarly journals Proliferation of Endothelial and Tumor Epithelial Cells by Progestin-Induced Vascular Endothelial Growth Factor from Human Breast Cancer Cells: Paracrine and Autocrine Effects

Endocrinology ◽  
2005 ◽  
Vol 146 (8) ◽  
pp. 3632-3641 ◽  
Author(s):  
Yayun Liang ◽  
Salman M. Hyder
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Vascular Endothelial ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Angiogenic Growth Factors ◽  
Endothelial Growth Factor

Abstract Angiogenesis, the formation of new blood vessels, is essential for tumor expansion, and vascular endothelial growth factor (VEGF) is one of the most potent angiogenic growth factors known. We have previously shown that natural and synthetic progestins, including those used in hormone replacement therapy and oral contraception, induce the synthesis and secretion of VEGF in a subset of human breast cancer cells in a progesterone receptor-dependent manner. We now report that conditioned medium from progestin-treated breast tumor cells can induce the proliferation of endothelial cells in a paracrine manner and induce the proliferation of tumor epithelial cells in a paracrine and an autocrine manner. The use of an anti-VEGF antibody and SU-1498, an inhibitor of VEGF receptor-2 (VEGFR-2 or flk/kdr) tyrosine kinase activity, demonstrated that these effects involve interactions between VEGF and VEGFR-2. Also, blockage of progestin-induced VEGF by the antiprogestin RU-486 (mifepristone) eliminated VEGF-induced proliferative effects. The ability of VEGF to increase the proliferation of endothelial cells and tumor cells, including those that do not release VEGF in response to progestins, suggests that these effects are mediated by amplification of the progestin signal, which culminates in angiogenesis and tumor growth. These novel findings suggest that targeting the release of VEGF from tumor epithelial cells as well as blocking interactions between VEGF and VEGFR-2 on both endothelial and tumor epithelial cells may facilitate the development of new antiangiogenic therapies for progestin-dependent breast tumors. Furthermore, these data indicate that it would be useful to develop selective progesterone receptor modulators that prevent the release of angiogenic growth factors from breast cancer cells.

Post-cyclosporine-mediated hypertension and nephropathy: amelioration by vascular endothelial growth factor

2001 ◽  
Vol 280 (4) ◽  
pp. F727-F736 ◽  
Author(s):  
Duk-Hee Kang ◽  
Yoon-Goo Kim ◽  
Takeshi F. Andoh ◽  
Katherine L. Gordon ◽  
Shin-Ichi Suga ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
High Salt ◽  
Vascular Endothelial ◽  
Tubulointerstitial Injury ◽  
Angiogenic Growth Factors ◽  
High Salt Diet ◽  
Salt Diet ◽  
Salt Sensitive Hypertension ◽  
Endothelial Growth Factor

Recent studies have demonstrated a role for microvascular and tubulointerstitial injury in some models of salt-sensitive hypertension. We utilized a model of post-cyclosporin A (CsA) nephropathy and hypertension to test the hypothesis that treatment with an angiogenic factor aimed at ameliorating the microvascular and renal injury would prevent the development of hypertension. CsA was administered with a low-salt diet for 45 days, resulting in a renal lesion characterized by afferent arteriolopathy, focal peritubular capillary loss, and tubulointerstitial fibrosis. Rats were then placed on a high-salt diet and randomized to receive either vascular endothelial growth factor (VEGF121) or vehicle for 14 days. Placement of rats with established CsA nephropathy on a high-salt diet results in the rapid development of salt-sensitive hypertension. VEGF121 treatment resulted in lower blood pressure, and this persisted on discontinuing the VEGF. VEGF121 treatment was also associated with a decrease in osteopontin expression, macrophage infiltration, and collagen III deposition and markedly stimulated resolution of the arteriolopathy (20.9 ± 7.8 vs. 36.9 ± 6.1%, VEGF vs. vehicle, P < 0.05). In conclusion, CsA-associated renal microvascular and tubulointerstitial injury results in the development of salt-sensitive hypertension. Treatment of animals with established CsA nephropathy with VEGF reduces the hypertensive response and accelerates histological recovery. The vascular protective effect of VEGF may be due to the improvement of arteriolopathy. Angiogenic growth factors may represent a novel strategy for treating CsA-associated hypertension and renal disease.

scholarly journals Angiogenesis during primate placentation in health and disease

Reproduction ◽  
2003 ◽  
pp. 569-577 ◽  
Author(s):  
C Wulff ◽  
M Weigand ◽  
R Kreienberg ◽  
HM Fraser
Keyword(s):  
Intrauterine Growth Retardation ◽  
Normal Development ◽  
Trophoblast Invasion ◽  
Vascular Endothelial ◽  
Angiogenic Growth Factors ◽  
Intrauterine Growth ◽  
Endothelial Cell Differentiation ◽  
Health And Disease ◽  
Endothelial Growth Factor ◽  
Proliferation And Invasion

Normal embryonic development is dependent upon a sufficient oxygen, nutrient and waste exchange through the placenta. In primates including humans, this exchange is attained by successful haemochorial placentation which requires the transformation of maternal intramyometrial spiral arterioles by trophoblast invasion to gain uteroplacental circulation, and establishment and maintenance of a competent fetoplacental vasculature. Thus, trophoblast and endothelial cell differentiation, proliferation and invasion occurring during placentation have to be tightly regulated. This review focuses on the diverse developmental steps during haemochorial placentation in humans and other primates and the possible involvement of angiogenic growth factors (vascular endothelial growth factor (VEGF) and angiopoietins (Ang)) in these processes, highlighting the importance of specific actions of angiogenic ligand-receptor pairs. It is hypothesized that VEGF/VEGF-R1 and Ang-1/Tie receptor 2 (Tie-2) may regulate trophoblast differentiation and invasion; VEGF/VEGF-R2 and Ang-1/Tie-2 may promote fetoplacental vascular development and stabilization; and Ang-2/Tie-2 may be involved in maternal vascular remodelling. The importance of a tight regulation of angiogenic factors and their endogenous antagonists for normal development of the placenta is demonstrated by failure of this system, resulting in abnormal placenta vascularization and trophoblast invasion associated with intrauterine growth retardation or pre-eclampsia.

Analysis of endothelial precursor cells in chronic migraine: A case-control study

Cephalalgia ◽  
2012 ◽  
Vol 33 (4) ◽  
pp. 236-244 ◽  
Author(s):  
Agustin Oterino ◽  
Maria Toriello ◽  
Enrique Palacio ◽  
Vicente G Quintanilla ◽  
Nuria Ruiz-Lavilla ◽  
...  
Keyword(s):  
Surrogate Marker ◽  
Vascular Risk Factor ◽  
Endothelial Activation ◽  
Endothelial Damage ◽  
Control Group ◽  
Vascular Endothelial ◽  
Circulating Cells ◽  
Colony Forming Units ◽  
Calcitonin Gene ◽  
Endothelial Growth Factor

Background: Migraine has been considered a vascular risk factor especially in young women. Factors predisposing to endothelial damage in migraine are still being debated. The insufficiency of circulating endothelial precursor circulating cells (EPCs) suggested a link between migraine and cardiovascular risk. This research aimed to study a subtype of EPCs, those expressing e-selectin, to assess endothelial activation and, therefore, endothelial dysfunction in migraine. Methods: Consecutive headache patients ( n = 99) and 35 adjusted controls were recruited. Total EPCs, defined as CD34+/KDR+ cells, and EPC colony-forming units (CFUs) were assayed. We identified as “early” EPCs those CD62E– EPCs, and “late” EPCs, CD62E+, a surrogate marker for endothelial damage. Plasmatic calcitonin-gene related protein (CGRP) and vascular-endothelial growth factor (VEGF) were analyzed. Results: We did not find differences in the total number of CFUs among clinical groups. Means of total CD34+/KDR+ and “early” EPCs were not significant among clinical groups. Nevertheless, the mean of “late” EPCs was lower (log10-transformed mean = 1.715; SD = 0.393) in the control group than in the migraine patients (log10-transformed mean = 2.167; SD = 0.685), even after adjustment by VEGF plasma level and other confounding factors. Linear regression analyses disclosed significant predictors for “late” EPCs for controls vs migraine (β = 0.452 SE ± 0.13; p = 0.001). We did not observe differences between migraine with or without aura. Conclusion: We observed higher number of activated EPCs in migraine patients than in controls. CD62E+ EPCs might be considered a marker for vascular damage in migraine patients.

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