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토끼 허혈성 하지 모델에서 VEGF 발현 Naked DNA 벡터인pCK-VEGF의 근육내 투여가 측부혈관형성에 미치는 영향
체제건(Jei Keon Chae),전현순(Hyun Sun Jeon),박은진(Eun Jin park),김종묵(Jong Mook Kim),김덕경(Duk Kyung Kim),김선영(Sun Young Kim) 대한약학회 2001 약학회지 Vol.45 No.1
We have recently reported the development of a high efficiency expression vector, pCK, which can drive a high level of gene expression in mouse skeletal muscle. In this study, we tested the therapeutic potential of pCK expressing human VEGF165, pCK-VEGF, in the rabbit ischemic hind limb model. To determine the optimal dose of plasmid DNA, various concentrations of pCK-CAT, were injected into the muscle of a rabbit hind limb and the levels of CAT activity were determined. It was found that the expression level of the exgenously added gene became stable between 250 and 1,000ug. Based on this result, we tested whether intramuscular transfer of 500ug of pCK-VEGF could actually modulate collateral vessel development in a rabbit ischemic hind limb model. It was found that reative to the control group injected with the pCK lacking the VEGF sequence, single intramuscular doses (500ug) of pCK-VEGF produced statistically significant augmentation of collateral vessels as determinde by the angiographic vessel count, maximal blood flow by Doppler flowmeter, and the number of capillaries by histology. These results suggest that a single 500ug-delivery of pCK-VEGF is potent enough to induce sufficient angiogenic activity and achieve therapeutic benefit on this rabbit model.
채제건 대한핵의학회 1999 핵의학 분자영상 Vol.33 No.2
Percutaneous Transluminal Coronary Angioplasty (PTCA) remains limited by restenosis that occurs in 30 to 50% of patients with coronary artery disease. During the last decade, numerous agents have been used to prevent restenosis. Despite positive results in animal models, no pharmacological therapy has been found to significantly decrease the risk of restenosis in humans. These discrepancies between animal models and clinical situation were probably related to an incomplete understanding of the mechanism of restenosis. Neointimal thickening occurs in response to experimental arterial injury with a balloon catheter. Neointimal formation involves different steps: smooth muscle cell activation, proliferation and migration, and the production of extracellular matrix. The factors that control neointimal hyperplasia include growth factors, humoral factors and mechanical factors. Arterial remodeling also plays a major role in the restenosis process. Studies performed in animal and human subjects have established the potentials for "constrictive remodeling" to reduce the post-angioplasty vessel area, thereby indirectly narrowing the vessel lumen and thus contributing to restenosis. The reduction of restenosis rate in patients with intracoronary stent implantation has been attributed to the preventive effect of stent itself for this negative remodeling. In addition to these mechanisms for restenosis, intraluminal or intra-plaque thrombus formation, reendothelialization and apoptosis theories have been introduced and confirmed at least in part.