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Angiogenic Gene Therapy for Experimental Critical Limb Ischemia: Acceleration of Limb Loss by Overexpression of Vascular Endothelial Growth Factor 165 but not of Fibroblast Growth Factor-2
VEGF is necessary, but should be delicately regulated to lower expression to treat ischemic limb, and the therapeutic effect of FGF-2, associated with the harmonized angiogenic effects seen with endogenous VEGF, provides important insights into therapeutic angiogenesis.
Efficient gene transfer to airway epithelium using recombinant Sendai virus
It is shown that recombinant Sendai virus (SeV) produces efficient transfection throughout the respiratory tract of both mice and ferrets in vivo, as well as in freshly obtained human nasal epithelial cells in vitro.
Fibroblast Growth Factor-2 Determines Severity of Joint Disease in Adjuvant-Induced Arthritis in Rats
It is shown that both polypeptides were up-regulated in the rat joint synovial tissue of an adjuvant-induced model of arthritis (AIA), as well as human subjects with RA, indicating direct in vivo evidence of disease-modulatory effects of FGF-2, as probably associated with endogenous VEGF function.
Transfer of wild-type p53 gene effectively inhibits vascular smooth muscle cell proliferation in vitro and in vivo.
In vivo transfection of p53 cDNA inhibited neointimal formation after balloon injury in rabbit carotid arteries, without apoptotic stimuli, and this novel concept, including not only exogenous but also endogenous p53 overexpression in the vessel wall, may be one approach worth exploring in the treatment of patients with restenosis occurring after vascular interventions.
Platelet-derived growth factor-AA is an essential and autocrine regulator of vascular endothelial growth factor expression in non-small cell lung carcinomas.
The PDGF-AA/VEGF axis may be a ubiquitous autocrine system for enhancing angiogenic signals, and PDGF -AA, and its related pathways could be a more efficient target of antiangiogenic therapy for cancers than VEGF and its pathways.
Spreds Are Essential for Embryonic Lymphangiogenesis by Regulating Vascular Endothelial Growth Factor Receptor 3 Signaling
It is demonstrated that the deletion of both Sp red-1 and Spred-2 resulted in embryonic lethality at embryonic days 12.5 to 15.5 with marked subcutaneous hemorrhage, edema, and dilated lymphatic vessels filled with erythrocytes, suggesting that Spreds play an important role in lymphatic vessel development by negatively regulating VEGF-C/VEGFR-3 signaling.
The Sprouty-related protein, Spred, inhibits cell motility, metastasis, and Rho-mediated actin reorganization
It is demonstrated that Spred1 inhibits the metastasis of LM8 cells in nude mice and suggests that the induction of Spreds could be a novel strategy for preventing cancer cell metastasis.