scholarly journals The Role of Cytokines, Chemokines, and Growth Factors in the Pathogenesis of Pityriasis Rosea

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Francesco Drago ◽  
Giulia Ciccarese ◽  
Francesco Broccolo ◽  
Massimo Ghio ◽  
Paola Contini ◽  
...  
Keyword(s):  
Growth Factors ◽  
Human Herpesvirus ◽  
Inflammatory Cells ◽  
Serum Levels ◽  
Vascular Endothelial ◽  
Healthy Controls ◽  
Pityriasis Rosea ◽  
Vasculogenesis And Angiogenesis ◽  
Endothelial Growth Factor

Introduction. Pityriasis rosea (PR) is an exanthematous disease related to human herpesvirus- (HHV-) 6/7 reactivation. The network of mediators involved in recruiting the infiltrating inflammatory cells has never been studied.Object. To investigate the levels of serum cytokines, growth factors, and chemokines in PR and healthy controls in order to elucidate the PR pathogenesis.Materials and Methods. Interleukin- (IL-) 1, IL-6, IL-17, interferon- (IFN-)γ, tumor necrosis factor- (TNF-)α, vascular endothelial growth factor (VEGF), granulocyte colony stimulating factor (G-CSF), and chemokines, CXCL8 (IL-8) and CXCL10 (IP-10), were measured simultaneously by a multiplex assay in early acute PR patients’ sera and healthy controls. Subsequently, sera from PR patients were analysed at 3 different times (0, 15, and 30 days).Results and discussion. Serum levels of IL-17, IFN-γ, VEGF, and IP-10 resulted to be upregulated in PR patients compared to controls. IL-17 has a key role in host defense against pathogens stimulating the release of proinflammatory cytokines/chemokines. IFN-γhas a direct antiviral activity promoting NK cells and virus specific T cells cytotoxicity. VEGF stimulates vasculogenesis and angiogenesis. IP-10 can induce chemotaxis, apoptosis, cell growth, and angiogenesis.Conclusions. Our findings suggest that these inflammatory mediators may modulate PR pathogenesis in synergistic manner.

scholarly journals Female sexual dysfunction in systemic sclerosis: The role of endothelial growth factor and endostatin

2018 ◽  
Vol 4 (1) ◽  
pp. 71-76 ◽  
Author(s):  
Antonietta Gigante ◽  
Luca Navarini ◽  
Domenico Margiotta ◽  
Biagio Barbano ◽  
Antonella Afeltra ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Blood Flow ◽  
Systemic Sclerosis ◽  
Growth Factor ◽  
Sexual Dysfunction ◽  
Resistive Index ◽  
Serum Levels ◽  
Vascular Endothelial ◽  
Healthy Controls ◽  
Endothelial Growth Factor

Introduction: Since female sexual dysfunction in systemic sclerosis women is multifactorial, we can assume that vascular damage may play a role in pathogenesis. The aim of the study was to evaluate the clitoral blood flow, by Echo color Doppler, and to correlate it whit serum levels of vascular endothelial growth factor and endostatin. Methods: A total of 15 systemic sclerosis women and 10 healthy controls matched for sex and age were enrolled in this study. Serum VEGF165 and endostatin levels were determined in systemic sclerosis patients by commercial enzyme-linked immunosorbent assay kit. Clitoral blood flow was measured by Doppler indices of clitoral artery: pulsatile index, resistive index, and systolic/diastolic ratio were measured. Sexual dysfunction was assessed by Female Sexual Function Index. Results: Vascular endothelial growth factor (pg/mL) and endostatin (ng/mL) median values were significantly higher in systemic sclerosis women than healthy controls. Resistive index and systolic/diastolic ratio median values were significantly higher in systemic sclerosis women than healthy controls. Negative correlation exists between serum levels of vascular endothelial growth factor and resistive index (r = −0.55, p < 0.05). Positive correlation was observed between serum levels of endostatin and resistive index (r = 0.70, p < 0.01) and systolic/diastolic ratio (r = 0.77, p < 0.01). Discussion: We can suppose that clitoral blood flow in systemic sclerosis women is reduced not only for macro- and microvascular damage but also for impaired angiogenesis.

Growth Factors and Their Corresponding Receptors as Targets for Ovarian Cancer Therapy

2018 ◽  
Author(s):  
Anca Maria Cimpean ◽  
Andreea Adriana Jitariu ◽  
Marius Raica
Keyword(s):  
Ovarian Cancer ◽  
Growth Factors ◽  
Growth Factor ◽  
Disease Free Survival ◽  
Endocrine Gland ◽  
Vascular Endothelial ◽  
Free Survival ◽  
Ovarian Carcinogenesis ◽  
Endothelial Growth Factor

Ovarian cancer remains one of the most aggressive and difficult to manage malignancies regarding evaluation and therapeutic options. The high mortality persists despite extensive research in the field. Current conventional chemotherapy does not improve disease-free survival and does not decrease recurrences amongst patients. This calls for a stringent reconsideration of the drugs selection, focused on the most targeted strategies and personalization of the therapy. Targeted agents against growth factors and their corresponding receptors are already approved as first- or second-line neoadjuvant therapy with controversial results. This chapter critically discusses the role of growth factors as vascular endothelial growth factor, fibroblast growth factors, or platelet-derived growth factors and their corresponding receptors in the pathogenesis, progression, and selection of therapeutic strategies. Other growth factors, such as nerve growth factor or endocrine gland derived growth factor, seem to have a strong involvement in ovarian carcinogenesis but their actual impact is not fully understood.

Serum Levels of Vascular Endothelial Growth Factor (VEGF) and Basic Fibroblast Growth Factor (bFGF) in Children with Acute Lymphoblastic Leukemia.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4387-4387
Author(s):  
Izabela Palgan ◽  
Mariusz Wysocki ◽  
Krzysztof Palgan ◽  
Robert Debski ◽  
Grazyna Odrowaz-Sypniewska ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Lymphoblastic Leukemia ◽  
Serum Levels ◽  
Control Group ◽  
Vascular Endothelial ◽  
Healthy Controls ◽  
Fibroblast Growth ◽  
Childhood All ◽  
Endothelial Growth Factor

Abstract Angiogenesis is a process of blood vessel formation from the preexisting capillaries. It plays an essential role of growth and development of cancer. The aim of this study was to evaluate serum levels of the most important angiogenic stimulators, Vascular Endothelial Growth Factor (VEGF) and basic Fibroblast Growth Factor (bFGF) in children with acute lymphoblastic leukemia (ALL) and their relation to clinical manifestations of the disease, and in healthy controls. Although VEGF and bFGF have been suggested to be reliable prognostic indicators and important tools for treatment approach in hematopoietic malignancies and solid tumors, experience in childhood ALL has been limited. Patients and methods: 46 children with ALL (24 male, 22 female) aged 2-18 years (median 8 years) at the time of diagnosis and in remission and 70 healthy children (31 male, 39 female). For the quantitative determination of human VEGF and bFGF, the Quantikine (R&D Systems, Minneapolis, MN, USA), a solid phase enzyme-linked immunosorbent assay method was used. Elevated VEGF and bFGF were defined as being higher than the 95 percentile value in control group. Results: The range of VEGF serum levels in healthy controls was 24.73–467.7 pg/ml (median 168.9 pg/ml), 95 percentile was 431.85 pg/ml and the range of bFGF serum levels was 0–10.8 pg/ml (median 2.9 pg/ml), 95 percentile was 6.95 pg/ml. In children with ALL, the range of VEGF serum levels at the time of diagnosis was 0–532.3 pg/ml (median 91.18 pg/ml), and bFGF 0–64.48 pg/ml (median 5.11 pg/ml). In children in remission, the range of serum levels of VEGF was 53.15–962.67 pg/ml (median 209.73 pg/ml), and bFGF 0–32.5 pg/ml (median 5.98 pg/ml). The median level of VEGF at diagnosis was lower than those of the control group (p=0.006), and higher in remission, when compared to values obtained in children on diagnosis and in the control group (p=0.0005; p=0.01). Elevated level of VEGF was observed in 8.7% children at the time of diagnosis and in 24.4% of patients in remission. The median levels of bFGF at diagnosis and in remission were significantly higher than those in control group with 40% of children having elevated levels. A positive correlation between VEGF serum concentration and platelet number, and negative correlation between VEGF serum levels and WBC were observed, with no other correlations between growth factors (VEGF, bFGF) and age, type of lymphoblasts (FAB), risk group, and drug resistance. Conclusion: These results suggest that bFGF more than VEGF can play an important role in childhood ALL. The serum levels of angiogenic factors may be related to the activity of the disease, while both growth factors can possibly be a target of anti-angiogenic therapy.

scholarly journals Circulating angiopoietin-2 is elevated in patients with neuroendocrine tumours and correlates with disease burden and prognosis

2009 ◽  
Vol 16 (3) ◽  
pp. 967-976 ◽  
Author(s):  
R Srirajaskanthan ◽  
G Dancey ◽  
A Hackshaw ◽  
T Luong ◽  
M E Caplin ◽  
...  
Keyword(s):  
Disease Burden ◽  
Neuroendocrine Tumour ◽  
Distant Metastases ◽  
Serum Levels ◽  
Serum Marker ◽  
Vascular Endothelial ◽  
Healthy Controls ◽  
Significant Difference ◽  
Angiopoietin 2 ◽  
Endothelial Growth Factor

Angiogenesis is an essential process in the development and growth of tumours. There are a large number of angiogenic mediators including the angiopoietin (Ang) family and vascular endothelial growth factor, which play an important role in both physiological and pathological angiogenesis. This study examines serum levels of Ang-1 and Ang-2 in patients with neuroendocrine tumour (NET) compared healthy controls. ELISA for Ang-1 and Ang-2 was performed in 47 patients with histologically proven NETs and 44 healthy controls. Immunohistochemical staining for Ang-2 was performed in patients to demonstrate cellular location of Ang-2. Serum Ang-2 levels were significantly elevated in patients compared controls (median 4756 vs 2495 pg/ml, P<0.001), while there was no significant difference in Ang-1 levels. The ratio of Ang-2:Ang-1 was significantly elevated in patients compared controls (0.13 vs 0.066, P<0.001). Serum Ang-2 levels were significantly elevated in patients with distant metastases compared with those without metastasis (median 5080 vs 3360 pg/ml, P=0.01). There was also a significant increase between Ang-2 levels and volume of liver metastases (P=0.014). Time to disease progression was worse in patients with serum Ang-2 levels >4756 pg/ml (P=0.04). Serum Ang-2 but not Ang-1 is elevated in NET patients. Ang-2 may be a useful serum marker for monitoring and assessment of prognosis in patients with NETs.

scholarly journals Critical role of CD11b+ macrophages and VEGF in inflammatory lymphangiogenesis, antigen clearance, and inflammation resolution

Blood ◽  
2009 ◽  
Vol 113 (22) ◽  
pp. 5650-5659 ◽  
Author(s):  
Raghu P. Kataru ◽  
Keehoon Jung ◽  
Cholsoon Jang ◽  
Hanseul Yang ◽  
Reto A. Schwendener ◽  
...  
Keyword(s):  
Critical Role ◽  
Lymphatic Vessels ◽  
Bacterial Pathogen ◽  
Inflammatory Cells ◽  
Vascular Endothelial ◽  
Factor C ◽  
Inflammation Resolution ◽  
Endothelial Growth Factor ◽  
Draining Lymph Nodes

Using a bacterial pathogen–induced acute inflammation model in the skin, we defined the roles of local lymphatic vessels and draining lymph nodes (DLNs) in antigen clearance and inflammation resolution. At the peak day of inflammation, robust expansion of lymphatic vessels and profound infiltration of CD11b+/Gr-1+ macrophages into the inflamed skin and DLN were observed. Moreover, lymph flow and inflammatory cell migration from the inflamed skin to DLNs were enhanced. Concomitantly, the expression of lymphangiogenic growth factors such as vascular endothelial growth factor C (VEGF-C), VEGF-D, and VEGF-A were significantly up-regulated in the inflamed skin, DLNs, and particularly in enriched CD11b+ macrophages from the DLNs. Depletion of macrophages, or blockade of VEGF-C/D or VEGF-A, largely attenuated these phenomena, and produced notably delayed antigen clearance and inflammation resolution. Conversely, keratin 14 (K14)–VEGF-C transgenic mice, which have dense and enlarged lymphatic vessels in the skin dermis, exhibited accelerated migration of inflammatory cells from the inflamed skin to the DLNs and faster antigen clearance and inflammation resolution. Taken together, these results indicate that VEGF-C, -D, and -A derived from the CD11b+/Gr-1+ macrophages and local inflamed tissues play a critical role in promoting antigen clearance and inflammation resolution.

PlGF and sVEGFR-1 in chronic subdural hematoma: implications for hematoma development

2013 ◽  
Vol 118 (2) ◽  
pp. 353-357 ◽  
Author(s):  
Theodosis Kalamatianos ◽  
Lampis C. Stavrinou ◽  
Christos Koutsarnakis ◽  
Christina Psachoulia ◽  
Damianos E. Sakas ◽  
...  
Keyword(s):  
Growth Factor ◽  
Subdural Hematoma ◽  
Chronic Subdural Hematoma ◽  
Serum Levels ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Pathological Angiogenesis ◽  
Enhanced Expression ◽  
Endothelial Growth Factor

Object A considerable body of evidence indicates that inflammation and angiogenesis play a significant role in the development and progression of chronic subdural hematoma (CSDH). While various experimental and clinical studies have implicated placental growth factor (PlGF) in the processes that underpin pathological angiogenesis, no study has thus far investigated its expression in CSDH. The actions of PlGF and its related proangiogenic vascular endothelial growth factor (VEGF) are antagonized by a high-affinity soluble receptor, namely soluble VEGF receptor–1 (sVEGFR-1), and thus the ratio between sVEGFR-1 and angiogenic factors provides an index of angiogenic capacity. Methods In the present study, using an automated electrochemiluminescence assay, levels of PlGF and sVEGFR-1 were quantified in serum and hematoma fluid obtained in 16 patients with CSDH. Results Levels of PlGF and sVEGFR-1 were significantly higher in hematoma fluid than in serum (p < 0.0001). In serum, levels of sVEGFR-1 were higher than those of PlGF (p < 0.0001), whereas in hematoma fluid this difference was not apparent. Furthermore, the ratio of sVEGFR-1 to PlGF was significantly lower in hematoma fluid than in serum (p < 0.0001). Conclusions Given previous evidence indicating a role for PlGF in promoting angiogenesis, inflammatory cell chemotaxis, and stimulation, as well as its ability to amplify VEGF-driven signaling under conditions favoring pathological angiogenesis, enhanced expression of PlGF in hematoma fluid suggests the involvement of this factor in the mechanisms of inflammation and angiogenesis in CSDH. Furthermore, a reduced ratio of sVEGFR-1 to PlGF in hematoma fluid is consistent with the proangiogenic capacity of CSDH. Future studies are warranted to clarify the precise role of PlGF and sVEGFR-1 in CSDH.

scholarly journals Growth factors and kinases in glioblastoma growth

2016 ◽  
Vol 2 (5) ◽  
pp. 248 ◽  
Author(s):  
Miguel Ángel Peña-Ortiz ◽  
Liliana Germán-Castelán ◽  
Aliesha González-Arenas
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Signaling Pathways ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Glycogen Synthase ◽  
Vascular Endothelial ◽  
Growth Factor Beta ◽  
Endothelial Growth Factor

<p>Glioblastoma multiforme (GBM) is the most aggressive type of brain cancer, having the highest invasion, migration, proliferation, and angiogenesis rates. Several signaling pathways are involved in the regulation of these processes including growth factors and their tyrosine kinase receptors, such as vascular endothelial growth factor (VEGF), transforming growth factor beta (TGFβ), fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), and insulin-like growth factor–I (IGF–I). Different kinases and regulators also participate in signaling pathways initiated by growth factors, such as mitogen-activated kinases (MAPK), protein kinases C (PKC), phosphatidylinositol-3 kinases (PI3K), protein kinase B (PKB or Akt), glycogen synthase kinase 3β (GSK3β), the mTOR complex, and Bcl-2. In this review, we will focus on the role of these proteins as possible therapeutic targets in GBM.</p>

scholarly journals Vascular endothelial growth factor role in predicting vascular disorders in pregnant with fetal growth restriction syndrome

2015 ◽  
Vol 96 (2) ◽  
pp. 220-223 ◽  
Author(s):  
E V Ul’yanina ◽  
I F Fatkullin
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factors ◽  
Growth Factor ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Blood Circulation ◽  
Growth Restriction ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

The review covers the up-to-date data of vascular endothelial growth factor role in forming of placental blood circulation in non-complicated pregnancy and in fetal growth retardation syndrome. It is shown that the normal trophoblast invasion to the spiral arteries wall in the myometrium and adequate remodeling of spiral arteries are essential for the normal fetal growth and development. The processes of blood vessels formation - vasculogenesis and angiogenesis - are described in detail. The process of angiogenesis regulation by growth factors and their receptors is reviewed. The importance of angiogenic and antiangiogenic factors coordinated action for the adequate placental microvasculature formation and normal fetal development is described. The growth factor complexes and their receptors formation processes and competition for receptor binding, as well as the role of placental growth factor in uteroplacental complex angiogenesis are analyzed. It is shown that the serum growth factors represent the mechanisms of pathologic reactions in placental insufficiency and fetal growth restriction syndrome. Special attention is given to the family of vascular endothelial growth factor as for the most important angiogenesis regulator. To determine the physiological role of vascular endothelial growth factor and to assess the its influence on angiogenesis and adequate uteroplacental and fetoplacental blood circulation formation, the features of vascular endothelial growth factor chemical structure are described. Determining the vascular endothelial growth factor in blood may be used to assess the mother-placenta-fetus system formation. The need for developing the criteria for choosing the optimal delivery term in pregnant with fetal growth restriction syndrome is discussed.

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