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.

Chronic Subdural Hematoma: Role of Vascular Endothelial Growth Factor and Craniotomy in Pathophysiology and Prevention of Recurrence

2017 ◽  
Vol 14 (01) ◽  
pp. 001-005
Author(s):  
Prabal Deb ◽  
Shashivadhanan Sundaravadhanan
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Subdural Hematoma ◽  
Chronic Subdural Hematoma ◽  
Vascular Endothelial ◽  
Vegf Expression ◽  
Immunohistochemical Examination ◽  
Endothelial Growth Factor ◽  
Prevention Of Recurrence

AbstractCurrent body of evidence suggests that the maintenance or enlargement of chronic subdural hematoma (cSDH) is caused by multiple factors. Inflammatory and vascular endothelial growth factor (VEGF)–induced accumulation of hematoma plays an important role in pathophysiology of cSDH. If neomembrane is implicated in the propagation of inflammatory mediators, excision of the culprit membrane becomes essential to treat and prevent recurrence of cSDH. This retrospective study was conducted in a service hospital where 48 cases of cSDH were operated in 2 years. Patients were evaluated clinically and radiologically. Surgical procedure offered included burr hole craniotomy (BHC), twist drill craniotomy (TDC), or craniotomy (Cr) with excision of neomembrane. Cr was offered whenever there was suspicion or evidence of reaccumulation, solid or calcified hematoma formation, nonobliteration of the subdural space, or numerous thick membranes as were demonstrated in imaging. In Cr maximum part of outer neomembrane was excised and margins were coagulated. The excised outer neomembrane was sent for immunohistochemical examination to assess the VEGF expression. Depending on the VEGF expression as seen on the microscope, these expressions were grouped into weak, moderate, or strong VEGF expression. The study showed that cSDH patients with neomembrane formation benefit from Cr. The strong VEGF expression from the excised neomembrane further strengthens the proinflammatory VEGF theory propagation of cSDH. It further proves that excision of the culprit membrane is essential to prevent recurrences.

scholarly journals Peran reseptor vascular endothelial growth factor (VEGF) pada konka hipertrofi disebabkan oleh rinitis alergi

2016 ◽  
Vol 46 (2) ◽  
pp. 129
Author(s):  
Indra Zachreini ◽  
Muhammad Nadjib Dahlan Lubis ◽  
Adi Koesoema Aman ◽  
Suprihati Suprihati
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Allergic Rhinitis ◽  
Growth Factor ◽  
Odds Ratio ◽  
Protective Factor ◽  
Case Control ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Latar belakang: Konka hipertrofi walaupun tidak mengancam jiwa, namun dapat menyebabkan gangguan kualitas hidup akibat sumbatan hidung. Patogenesis terjadinya konka hipertrofi adalah akibat airway remodelling terutama pada konka nasal inferior. Vascular endothelial growth factor (VEGF) merupakan salah satu faktor angiogenik yang berperan dalam proses neovaskularisasi. Bagaimana peran angiogenik reseptor VEGF pada konka hipertrofi yang terjadi pada rinitis alergi, sampai saat ini belum jelas dan belum banyak diteliti. Tujuan: Mengetahui peran VEGF sebagai faktor angiogenesis pada konka hipertrofi yang terjadi pada rinitis alergi. Metode: Penelitian ini bersifat observasional analitik dengan rancangan case control pada sampel penelitian yang memenuhi kriteria inklusi. Reseptor VEGF diperiksa secara imunohistokimia, di mana nilainya terdiri dari nilai negatif dan positif. Hasil: Pada penelitian ini, didapati nilai odds ratio 0,11 dan 95% CI 0,013-0,982. Hal tersebut menunjukkan bahwa reseptor VEGF berperan sebagai faktor protektif pada konka hipertrofi yang terjadi pada rinitis alergi. Kesimpulan: Reseptor VEGF dianggap berperan sebagai faktor protektif terjadinya konka hipertrofi yang terjadi pada rinitis alergi.Kata kunci: Reseptor vascular endothelial growth factor, konka nasal hipertrofi, rinitis alergi, imunohistokimia ABSTRACT Background: Although hypertrophic turbinate is not life threatening, this condition often decreases quality of life, resulted from nasal obstruction. Pathogenesis of hypertrophic turbinate resulted from airway remodeling especially in inferior turbinate. Vascular endothelial growth factor (VEGF) is one of angiogenic factors which has a role in neovascularitation process. However, it is still unclear what is the role of VEGF receptor in angiogenic of allergic rhinitis, and until now there were very few studies about this matter. Purpose: To identify the role of VEGF as an angiogenic factor in hypertrophic turbinate caused by allergic rhinitis. Methods: This study was an analytical observation by case control method. VEGF receptors were examined by immunohistochemistry with negative and positive result. Result: This study found odds ratio 0.11 and 95% CI 0.013-0.982, which means that VEGF receptor was a protective factor in hypertrophic turbinate caused by allergic rhinitis. Conclusion: VEGF receptor was considered as a protective factor for the occurrence hypertrophic turbinate caused by allergic rhinitis.Keywords: Vascular endothelial growth factor receptor, hypertrophic turbinate, allergic rhinitis, immunohistochemistry

scholarly journals Melatonin Reduces Angiogenesis in Serous Papillary Ovarian Carcinoma of Ethanol-Preferring Rats

2017 ◽  
Author(s):  
Luiz Gustavo De Almeida Chuffa ◽  
Yohan Ricci Zonta ◽  
Marcelo Martinez ◽  
Isabel Cristina Cherici Camargo ◽  
Raquel Fantin Domeniconi ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Hypoxia Inducible Factor ◽  
Serum Levels ◽  
Ethanol Consumption ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Chemically Induced ◽  
Therapeutic Opportunity ◽  
Endothelial Growth Factor

Angiogenesis is a hallmark of ovarian cancer (OC) it promotes rapid cell growth and the associated metastasis. Identifying new bioactive compounds to target angiogenesis may provide valuable paradigms as therapeutic strategies. Melatonin is a well-characterized indoleamine that possesses important anti-angiogenic properties in a set of aggressive solid tumors. Herein, we evaluated the role of melatonin therapy on the angiogenic signaling pathway in OC of an ethanol-preferring rat model that mimics the same pathophysiological conditions occurring in women. OC was chemically induced with a single injection of 7,12-dimethylbenz(a)anthracene (DMBA) under the ovarian bursa. After the rats developed serous papillary OC, half of the animals received i.p. injections of melatonin (200 &micro;g/100 g body weight/day) for 60 days. Serum levels of melatonin were higher following therapy, and the expression of its receptor MT1R was significantly increased in OC-bearing rats, regardless of ethanol intake. TGFB1, a transforming growth factor-beta1, was reduced only after melatonin treatment. Importantly, vascular endothelial growth factor (VEGF) was severely reduced after melatonin therapy in animals given or not given ethanol. Conversely, the levels of VEGF receptor 1 (VEGFR1) was diminished after ethanol consumption, regardless of melatonin therapy, and VEGFR2 was only reduced following melatonin. Hypoxia-inducible factor (HIF)-1&alpha; was augmented with ethanol consumption, and notably, melatonin significantly reduced their levels. Collectively, our results suggest that melatonin attenuates angiogenesis in OC of an animal model of ethanol consumption; this provides a possible complementary therapeutic opportunity for concurrent OC chemotherapy.

scholarly journals Capillary Morphogenesis gene 2 mediates multiple pathways of growth factor-induced angiogenesis by regulating endothelial cell chemotaxis

2019 ◽  
Author(s):  
Lorna Cryan ◽  
Tsz-Ming Tsang ◽  
Jessica Stiles ◽  
Lauren Bazinet ◽  
Sai Lun Lee ◽  
...  
Keyword(s):  
Growth Factor ◽  
Corneal Neovascularization ◽  
Tube Formation ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
The Novel ◽  
Capillary Morphogenesis ◽  
Pathological Angiogenesis ◽  
Endothelial Tube Formation ◽  
Endothelial Growth Factor

AbstractPathological angiogenesis contributes to diseases as varied as cancer and corneal neovascularization. The vascular endothelial growth factor (VEGF) - VEGF receptor 2 (KDR/VEGFR2) axis has been the major target for treating pathological angiogenesis. However, VEGF-targeted therapies exhibit reduced efficacy over time, indicating that new therapeutic strategies are needed. Therefore, identifying new targets that mediate angiogenesis is of great importance. Here, we report that one of the anthrax toxin receptors, capillary morphogenesis gene 2 (ANTXR2/CMG2), plays an important role in mediating angiogenesis induced by both bFGF and VEGF. Inhibiting physiological ligand binding to CMG2 results in significant reduction of corneal neovascularization, endothelial tube formation and cell migration. We also report the novel finding that CMG2 mediates angiogenesis by regulating the direction of endothelial chemotactic migration without affecting overall cell motility.

scholarly journals Vascular Endothelial Growth Factor: Much More than an Angiogenesis Factor

2010 ◽  
Vol 21 (3) ◽  
pp. 377-379 ◽  
Author(s):  
Donald R. Senger
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Neural Cell ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Angiogenesis Factor ◽  
Therapeutic Goal ◽  
Pathological Angiogenesis ◽  
Cell Compartments ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF) is best known as a cytokine essential for embryonic vasculogenesis and for the angiogenesis associated with various pathologies including cancer. However, VEGF also serves other functions that are less widely recognized. An early study ( Berse et al., 1992 ) revealed widespread expression of VEGF transcripts in adult tissues devoid of ongoing neovascularization, thereby predicting additional VEGF functions distinct from angiogenesis. More recent studies have confirmed that VEGF does indeed serve multiple additional functions, including normal maintenance of endothelial and neural cell compartments. These findings have important implications for the use of VEGF antagonists and VEGF receptor antagonists in patients for which inhibition of pathological angiogenesis is the therapeutic goal.

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