Tissue‐inhibitors of metalloproteinase‐1 and vascular‐endothelial growth‐factor in severe haemophilia A children on low dose prophylactic recombinant factor VIII: Relation to subclinical arthropathy

Haemophilia ◽  
2020 ◽  
Vol 26 (4) ◽  
pp. 607-614
Author(s):  
Nevine Gamal Andrawes ◽  
Hossam Mousa Saker ◽  
Nouran Yousef Salah El‐Din ◽  
Mervat Abd Elhakim Hussain
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Factor Viii ◽  
Low Dose ◽  
Recombinant Factor Viii ◽  
Haemophilia A ◽  
Vascular Endothelial ◽  
Severe Haemophilia ◽  
Tissue Inhibitors Of Metalloproteinase ◽  
Endothelial Growth Factor

Low-dose X-ray irradiation promotes fracture healing through up-regulation of vascular endothelial growth factor

2010 ◽  
Vol 75 (6) ◽  
pp. 522-524 ◽  
Author(s):  
Xiang-Sheng Song ◽  
Xiao-Zhong Zhou ◽  
Ge Zhang ◽  
Qi-Rong Dong ◽  
Ling Qin
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Fracture Healing ◽  
Low Dose ◽  
Vascular Endothelial ◽  
X Ray ◽  
Endothelial Growth Factor

scholarly journals Chronic Low-Dose Alcohol Consumption Promotes Cerebral Angiogenesis in Mice

2021 ◽  
Vol 8 ◽  
Author(s):  
Jiyu Li ◽  
Chun Li ◽  
Ethyn G. Loreno ◽  
Sumitra Miriyala ◽  
Manikandan Panchatcharam ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Ischemic Stroke ◽  
Growth Factor ◽  
Alcohol Consumption ◽  
Low Dose ◽  
Vascular Endothelial ◽  
Chronic Alcohol ◽  
Chronic Alcohol Consumption ◽  
Physiological Conditions ◽  
Endothelial Growth Factor

Chronic alcohol consumption dose-dependently affects the incidence and prognosis of ischemic stroke. We determined the influence of chronic alcohol consumption on cerebral angiogenesis under physiological conditions and following ischemic stroke. In in vitro studies, acute exposure to low-concentration ethanol significantly increased angiogenic capability and upregulated vascular endothelial growth factor A (VEGF-A) and vascular endothelial growth factor receptor 2 (VEGFR2) in C57BL/6J mouse brain microvascular endothelial cells (MBMVECs). The increased angiogenic capability was abolished in the presence of a VEGFR2 inhibitor. In addition, the increased angiogenic capability and upregulated VEGF-A and VEGFR2 remained in chronically low-concentration ethanol-exposed MBMVECs. In in vivo studies, 8-week gavage feeding with low-dose ethanol significantly increased vessel density and vessel branches and upregulated VEGF-A and VEGFR2 in the cerebral cortex under physiological conditions. Furthermore, vessel density, vessel branches, and expression of VEGF-A and VEGFR2 in the peri-infarct cortex were significantly greater in low-dose ethanol-fed mice at 72 h of reperfusion. Although low-dose ethanol did not alter cerebral vasoreactivity and regional cerebral blood flow (rCBF) either before or during ischemia, it significantly augmented post-ischemic hyperemia during reperfusion. In contrast, exposure to high-concentration ethanol and 8-week gavage feeding with high-dose ethanol only had a mild inhibitory effect on angiogenic capability and cerebral angiogenesis, respectively. We conclude that heavy alcohol consumption may not dramatically alter cerebral angiogenesis, whereas light alcohol consumption significantly promotes cerebral angiogenesis.

Encapsulated vascular endothelial growth factor—secreting cell grafts have neuroprotective and angiogenic effects on focal cerebral ischemia

2005 ◽  
Vol 103 (1) ◽  
pp. 104-114 ◽  
Author(s):  
Akimasa Yano ◽  
Tetsuro Shingo ◽  
Akira Takeuchi ◽  
Takao Yasuhara ◽  
Kazuki Kobayashi ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Cerebral Ischemia ◽  
Growth Factor ◽  
Low Dose ◽  
Focal Cerebral Ischemia ◽  
Control Cell ◽  
Vascular Endothelial ◽  
Bhk Cells ◽  
Behavioral Studies ◽  
Endothelial Growth Factor

Object The authors evaluated the neuroprotective and angiogenic effects of a continuous and low-dose infusion of vascular endothelial growth factor (VEGF)-165 on cerebral ischemia in rats. Methods The authors introduced VEGF complementary (c)DNA into baby hamster kidney (BHK) cells and established a cell line that produces human VEGF165 (BHK-VEGF). The BHK-VEGF cells and BHK cells that had been transfected with an expression vector that did not contain human VEGF165 cDNA (BHK-control) were encapsulated. Both capsules were implanted into rat striata. Six days after capsule implantation, the right middle cerebral artery (MCA) was occluded. Some animals were killed 24 hours after occlusion to measure the volume of the resulting infarct and to perform immunohistochemical studies. Other animals were used for subsequent behavioral studies 1, 7, and 14 days after MCA occlusion. The encapsulated BHK-VEGF cell grafts significantly reduced the volume of the infarct and the number of apoptotic cells in the penumbral area when compared with the effect of the BHK-control cell capsule. In addition, angiogenesis and gliogenesis significantly increased in the region around the capsule in animals that received BHK-VEGF cell capsules without an increase in focal cerebral blood flow; this did not occur in animals that received the BHK-control cell capsule. In behavioral studies rats that received the BHK-VEGF cell capsule displayed significant recovery while participating in the accelerating rotarod test after stroke. Conclusions Continuous intracerebral administration of low-dose VEGF165 through encapsulated grafts of VEGF-producing cells produces neuroprotective and angiogenic effects. These effects improve subsequent motor function.

scholarly journals The Effect of Venous Thromboembolism on Survival of Cancer Patients and its Relationship with Serum Levels of Factor VIII and Vascular Endothelial Growth Factor: A Prospective Matched-Paired Study

2006 ◽  
Vol 21 (4) ◽  
pp. 206-210 ◽  
Author(s):  
M. Dogan ◽  
A. Demirkazik ◽  
N. Konuk ◽  
B. Yalcin ◽  
A. Buyukcelik ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Venous Thromboembolism ◽  
Growth Factor ◽  
Factor Viii ◽  
Cancer Patients ◽  
Control Group ◽  
Vascular Endothelial ◽  
Plasma Factor ◽  
Endothelial Growth Factor ◽  
D Dimer

Background Venous thromboembolism (VT) increases mortality and morbidity in cancer patients. The primary aim of this study was to evaluate the effect of VT on the survival of cancer patients and its relationship with serum vascular endothelial growth factor (VEGF) and plasma factor VIII levels. Patients and methods Eighty-two patients with locally advanced or metastatic cancer were included in this study between September 2001 and March 2004, and 31 of them had VT. Fifty-one matched-paired cancer patients without VT were prospectively selected as a control group in the same period. Criteria for the selection of control group patients were having the same malignancy, stage, metastatic site, performance status and age (±5 years) as patients in the VT group. Results Plasma factor VIII and serum D-dimer levels in the VT group were significantly higher than those in the control group (p=0.030 and p=0.016, respectively). However, mean serum VEGF levels were similar in both groups (p=0.199). In the VT group, the median survival of patients who had higher serum VEGF levels (>150 pg/mL) was significantly shorter than that of patients in the same group with lower serum VEGF levels (p=0.005). The median survival of the VT group was 14 months, whereas it was 25 months in the control group (p=0.199). Conclusion There was a worse prognostic trend for cancer patients with VT. Nevertheless, the difference in survival was not statistically significant between the groups. Plasma factor VIII and serum D-dimer levels might have prognostic value in cancer patients with VT. Cancer patients with VT and higher serum VEGF levels had a significantly poorer prognosis.

Expression of vascular endothelial growth factor (VEGF) and factor VIII in the gilt placenta and its relation to fetal development

2017 ◽  
Vol 92 ◽  
pp. 63-68 ◽  
Author(s):  
Gregório C. Guimarães ◽  
Lorena A. Alves ◽  
Rafael P. Betarelli ◽  
Camila S.O. Guimarães ◽  
Fernanda R. Helmo ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Factor Viii ◽  
Fetal Development ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

scholarly journals Low-Dose Dopamine Agonist Administration Blocks Vascular Endothelial Growth Factor (VEGF)-Mediated Vascular Hyperpermeability without Altering VEGF Receptor 2-Dependent Luteal Angiogenesis in a Rat Ovarian Hyperstimulation Model

Endocrinology ◽  
2006 ◽  
Vol 147 (11) ◽  
pp. 5400-5411 ◽  
Author(s):  
Raul Gomez ◽  
Miguel Gonzalez-Izquierdo ◽  
Ralf C. Zimmermann ◽  
Edurne Novella-Maestre ◽  
Isabel Alonso-Muriel ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Low Dose ◽  
Specific Treatment ◽  
Vegf Receptor ◽  
Ovarian Hyperstimulation ◽  
Mrna Levels ◽  
Vascular Endothelial ◽  
Serum Progesterone ◽  
Endothelial Growth Factor

No specific treatment is available for ovarian hyperstimulation syndrome (OHSS), the most important complication in infertile women treated with gonadotropins. OHSS is caused by increased vascular permeability (VP) through ovarian hypersecretion of vascular endothelial growth factor (VEGF)-activating VEGF receptor 2 (VEGFR-2). We previously demonstrated in an OHSS rodent model that increased VP was prevented by inactivating VEGFR-2 with a receptor antagonist (SU5416). However, due to its toxicity (thromboembolism) and disruption of VEGFR-2-dependent angiogenic processes critical for pregnancy, this kind of compound cannot be used clinically to prevent OHSS. Dopamine receptor 2 (Dp-r2) agonists, used in the treatment of human hyperprolactinemia including pregnancy, inhibit VEGFR-2-dependent VP and angiogenesis when administered at high doses in animal cancer models. To test whether VEGFR-2-dependent VP and angiogenesis could be segregated in a dose-dependent fashion with the Dp-r2 agonist cabergoline, a well-established OHSS rat model supplemented with prolactin was used. A 100 μg/kg low-dose Dp-r2 agonist cabergoline reversed VEGFR-2-dependent VP without affecting luteal angiogenesis through partial inhibition of ovarian VEGFR-2 phosphorylation levels. No luteolytic effects (serum progesterone levels and luteal apoptosis unaffected) were observed. Cabergoline administration also did not affect VEGF/VEGFR-2 ovarian mRNA levels. Results in the animal model and the safe clinical profile of Dp-r2 agonists encouraged us to administer cabergoline to oocyte donors at high risk for developing the syndrome. Prophylactic administration of cabergoline (5–10 μg/kg·d) decreased the occurrence of OHSS from 65% (controls) to 25% (treatment). Therefore, a specific, safe treatment for OHSS is now available.

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