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Expressing VEGF (expressing + vegf)

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Medical Sciences	100%

Selected Abstracts

Cartilage repair in a rat model of osteoarthritis through intraarticular transplantation of muscle-derived stem cells expressing bone morphogenetic protein 4 and soluble flt-1

ARTHRITIS & RHEUMATISM, Issue 5 2009
Tomoyuki Matsumoto
Objective The control of angiogenesis during chondrogenic differentiation is an important issue affecting the use of stem cells in cartilage repair, especially with regard to the persistence of regenerated cartilage. This study was undertaken to investigate the effect of vascular endothelial growth factor (VEGF) stimulation and the blocking of VEGF with its antagonist, soluble Flt-1 (sFlt-1), on the chondrogenesis of skeletal muscle-derived stem cells (MDSCs) in a rat model of osteoarthritis (OA). Methods We investigated the effect of VEGF on cartilage repair in an immunodeficiency rat model of OA after intraarticular injection of murine MDSCs expressing bone morphogenetic protein 4 (BMP-4) in combination with MDSCs expressing VEGF or sFlt-1. Results In vivo, a combination of sFlt-1, and BMP-4,transduced MDSCs demonstrated better repair without osteophyte formation macroscopically and histologically following OA induction, when compared with the other groups. Higher differentiation/proliferation and lower levels of chondrocyte apoptosis were also observed in sFlt-1, and BMP-4,transduced MDSCs compared with a combination of VEGF- and BMP-4,transduced MDSCs or with BMP-4,transduced MDSCs alone. In vitro experiments with mixed pellet coculture of MDSCs and OA chondrocytes revealed that BMP-4,transduced MDSCs produced the largest pellets, which had the highest gene expression of not only type II collagen and SOX9 but also type X collagen, suggesting formation of hypertrophic chondrocytes. Conclusion Our results demonstrate that MDSC-based therapy involving sFlt-1 and BMP-4 repairs articular cartilage in OA mainly by having a beneficial effect on chondrogenesis by the donor and host cells as well as by preventing angiogenesis, which eventually prevents cartilage resorption, resulting in persistent cartilage regeneration and repair. [source]

Angiogenic gene modification of skeletal muscle cells to compensate for ageing-induced decline in bioengineered functional muscle tissue

BJU INTERNATIONAL, Issue 7 2008
Dawn M. Delo
OBJECTIVE To explore the effects of ageing on the viability of bioengineered striated muscle tissue in vivo, and if this viability can be enhanced by concurrent neovascularization, as its utility for the treatment of stress urinary incontinence (SUI) might be reduced if muscle cells are derived from old patients. MATERIALS AND METHODS Myoblasts were obtained and expanded in culture from young (2 weeks), mature (3 months) and old (24 months) mice, and were engineered to express vascular endothelial growth factor (VEGF) to stimulate neovascularization. Myoblasts were injected subcutaneously into male nude mice and after 2 and 4 weeks, the engineered muscle tissues were harvested. RESULTS Bioengineered muscle tissues were formed in all groups, but the engineered muscles formed by myoblasts from old mice were smaller and less contractile. However, the bioengineered muscles expressing VEGF had a greater mass and better contractility in all age groups. CONCLUSION This pilot study showed that there was an age-related decline in the size and function of bioengineered muscle; however, there was an improvement in volume and function when the muscle cells were expressing VEGF. [source]

The role of arachidonic acid metabolites in DR

ACTA OPHTHALMOLOGICA, Issue 2008
AM ABU EL ASRAR
Purpose The inducible enzyme cyclooxygense-2 (COX-2) and its metabolic products are important mediators for angiogenesis. We investigated the expression of COX-2 and its downstream enzymes microsomal prostaglandin-E synthase (mPGES)-1, cytosolic PGES (cPGES) and thromboxane synthase (TXS) and correlated it with vascular endothelial growth factor (VEGF) expression and level of vascularization in proliferative diabetic retinopathy (PDR) epiretinal membranes. Methods Fourteen membranes were studied by immunohistochemistry. Results Vascular endothelial cells expressed COX-2, mPGES-1 and VEGF in 75.6%, 64.3% and 50% of the membranes, respectively. TXS was expressed in stromal cells in 85.7% of the membranes. There was no immunoreactivity for cPGES. There were significant correlations between number of blood vessels expressing CD34 and the numbers of blood vessels expressing COX-2 (rs = 0.858; p<0.001), mPGES-1 (rs = 0.743; p = 0.002) and VEGF (rs = 0.845; p = 0.001) and the number of cells expressing TXS (rs = 0.74; p = 0.002). Number of blood vessels expressing VEGF correlated significantly with the numbers of blood vessels expressing COX-2 (rs = 0.879; p<0.001) and mPGES-1 (rs = 0.942; p<0.001) and the number of cells expressing TXS (rs = 0.702; p = 0.011). Conclusion COX-2 and its metabolic products might contribute to PDR angiogenesis. [source]

Vascular endothelial growth factor in nasal polyps: a comparison of asthmatic and non-asthmatic patients

CLINICAL OTOLARYNGOLOGY, Issue 6 2004
N.D. Bateman
The cause of nasal polyps remains unknown, although there is a well-recognized clinical association between nasal polyposis and asthma. The characteristic histological features of nasal polyps include large quantities of extracellular fluid. Vascular endothelial growth factor (VEGF) is a potent mediator of angiogenesis and vascular permeability. This study aimed to compare expression of VEGF in nasal polyps from patients with asthma and those with no apparent respiratory disease. Twenty-four asthmatic and 35 non-asthmatic patients were studied using immunohistochemistry for VEGF. VEGF expression was identified in endothelial, inflammatory and epithelial cells. There was significantly greater endothelial expression of VEGF in asthmatic patients (P < 0.05). Greater epithelial expression was observed in asthmatic patients but this did not reach statistical significance (P = 0.07). There was no difference in the density of inflammatory cells expressing VEGF. Differences between the two groups may reflect differences in disease severity or in the nature of the inflammatory process. [source]