Comparative Effects of Basic Fibroblast Growth Factor and Vascular Endothelial Growth Factor on Coronary Collateral Development and the Arterial Response to Injury

Lazarous, Daisy F.; Shou, Magang; Scheinowitz, Mickey; Hodge, Everett; Thirumurti, Venugopal; Kitsiou, Anastasia; Stiber, Jonathan A.; Lobo, Arlene; Hunsberger, Sally; Guetta, Esther; Epstein, Stephen E.; Unger, Ellis F.

doi:10.1161/01.cir.94.5.1074

Cited by 345 publications

(188 citation statements)

References 34 publications

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“…Different studies have shown that higher levels of bFGF are present in cardiac and skeletal muscle tissues after ischemia. [21][22][23] Recombinant bFGF was reported to enhance angiogenesis and collateral vessel formation following acute arterial occlusion and to result in the salvage of infarcted myocardium in canine models. 24,25 Basic FGF treatment of acute ischemic hindlimbs in rabbit or rat models using arterial ligation enhances angiogenesis, collateral vessel development, and muscle function.…”

Section: Discussionmentioning

confidence: 99%

Angiogenesis induced in muscle by a recombinant adenovirus expressing functional isoforms of basic fibroblast growth factor

et al. 1999

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Section: Discussionmentioning

confidence: 99%

Angiogenesis induced in muscle by a recombinant adenovirus expressing functional isoforms of basic fibroblast growth factor

et al. 1999

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“…Gene Therapy (2001) 8, 523-533. dial and limb ischemia. [4][5][6][7][8] In light of these results, clinicians have begun evaluating the therapeutic potential of various angiogenic factors in patients. 9 The recent failure of a clinical trial targeting the ischemic heart, where recombinant VEGF 165 protein was administered by a combination of intercoronary and intravenous injections, 10 has highlighted the need for alternative methods of delivering angiogenic factors in a chronic and sitespecific manner.…”

Section: Introductionmentioning

confidence: 99%

Delivery of FGF-2 but not VEGF by encapsulated genetically engineered myoblasts improves survival and vascularization in a model of acute skin flap ischemia

et al. 2001

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Stimulating angiogenesis by gene transfer approaches offers the hope of treating tissue ischemia which is untreatable by currently practiced techniques of vessel grafting and bypass surgery. Vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (FGF-2) are potent angiogenic molecules, making them ideal candidates for novel gene transfer protocols designed to promote new blood vessel growth. In this study, an ex vivo gene therapy approach utilizing cell encapsulation was employed to deliver VEGF and FGF-2 in a continuous and localized manner. C(2)C(12) myoblasts were genetically engineered to secrete VEGF(121), VEGF(165) and FGF-2. These cell lines were encapsulated in hollow microporous polymer membranes for transplantation in vivo. Therapeutic efficacy was evaluated in a model of acute skin flap ischemia. Capsules were positioned under the distal, ischemic region of the flap. Control flaps showed 50% necrosis at 1 week. Capsules releasing either form of VEGF had no effect on flap survival, but induced a modest increase in distal vascular supply. Delivery of FGF-2 significantly improved flap survival, reducing necrosis to 34.2% (P < 0.001). Flap vascularization was significantly increased by FGF-2 (P < 0.01), with numerous vessels, many of which had a large lumen diameter, growing in the proximity of the implanted capsules. These results demonstrate that FGF-2, delivered from encapsulated cells, is more efficacious than either VEGF(121) or VEGF(165) in treating acute skin ischemia and improving skin flap survival. Furthermore, these data attest to the applicability of cell encapsulation for the delivery of angiogenic factors for the treatment and prevention of tissue ischemia

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“…bFGF is an angiogenic peptide that may have many effects in vivo. It stimulates hematopoiesis (9) and it is a pluripotent mitogen of mesodermally derived cells and could theoretically exacerbate neointimal smooth muscle hyperplasia that could cause stenosis (10). bFGF also promotes the formation of new blood vessels.…”

Section: Discussionmentioning

confidence: 99%

ADP activation induces bFGF binding to platelets in vitro

Åkerblom

Lindahl

Larsson

2002

Upsala Journal of Medical Sciences

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Basic fibroblast growth factor (bFGF), is a heparin-binding factor with potent angiogenic properties in vitro and in vivo. bFGF is involved in tumour growth, but it has also been shown to reduce infarct size in experimentally induced acute myocardial infarction. Platelets are also believed to have an important role in both tumour growth and myocardial infarction.We have studied bFGF binding to platelets by flow cytometry. Platelet activation by ADP induces bFGF binding to platelets. bFGF bound to activated platelets will result in a locally high concentration of bFGF in patients with myocardial infarctions and malignant tumours. Addition of recombinant bFGF to platelet rich plasma reduced the percentage of fibrinogen positive platelets. bFGF may thus have an inhibitory effect on platelet aggregation.

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Comparative Effects of Basic Fibroblast Growth Factor and Vascular Endothelial Growth Factor on Coronary Collateral Development and the Arterial Response to Injury

Cited by 345 publications

References 34 publications

Angiogenesis induced in muscle by a recombinant adenovirus expressing functional isoforms of basic fibroblast growth factor

Angiogenesis induced in muscle by a recombinant adenovirus expressing functional isoforms of basic fibroblast growth factor

Delivery of FGF-2 but not VEGF by encapsulated genetically engineered myoblasts improves survival and vascularization in a model of acute skin flap ischemia

ADP activation induces bFGF binding to platelets in vitro

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