请高手帮忙，，感激不尽。。急用。。

夜*城

这是关于早期反应生长因子（EGR-1）的一段文章。请高手帮忙，谢谢了，，小弟急用，，Almost a decade ago we demonstrated by in situ hybridization that Egr-1 is rapidly (within hours) and transiently induced at the endothelial wound edge following balloon catheter scrape injury to the aortae of rats. In the same (endothelial denudation) model, we found that Egr-1 is expressed later by migrating SMCs. The expression and nuclear translocation of Egr-1 after mechanical injury is, at least in vitro, dependent on the release of endogenous FGF-2 and its paracrine activation of MEK/ERK-dependent signaling. FGF-2, a potent agonist of Egr-1, plays an important role vascular repair after injury. FGF-2 is locally and transiently (within minutes) released in the coronary arteries of humans undergoing stenting. SMC migration in rats after deendothelialization is augmented by systemic administration of FGF-2 and blocked by infusion of neutralizing antibodies to FGF-2.
That Egr-1 plays a critical role as a mediator of SMC growth and intimal thickening in the reparative response to vascular injury has been demonstrated using a variety of synthetic nucleic acid-based gene-silencing approaches. For example, antisense oligonucleotides (15-mers) with phosphorothioate linkages targeting various regions in rat Egr-1 mRNA, unlike random, scrambled, sense or mismatch versions, blocked primary aortic SMC replication and regrowth after in vitro scraping injury. Catalytic 34-mer DNA molecules (DNAzyme ED5) which target and degrade rat Egr-1 mRNA, also inhibited SMC growth and repair in vitro and, when delivered adventitially to rat common carotid arteries, suppressed Egr-1 protein expression after 1 hour and intimal thickening 14 days after balloon angioplasty. ED5 also blocks neointima formation in rat carotid arteries 18 days after permanent ligation.52 The DNAzyme has since been used to suppress the development of other proliferative states. For example, ED5 reduces cortical Egr-1 mRNA expression and interstitial fibrosis in rats 7 days after renal obstruction (unilateral ureteral ligation) and delivery by electroporation. In this model, the DNAzyme inhibited TGF-ß,  -SM-actin and type I collagen mRNA expression.
DNAzymes targeting the human version of Egr-1, which also inhibit Egr-1 expression and proliferation of human and porcine aortic SMCs, reduce in-stent restenosis in pig coronary arteries 30 days after endoluminal delivery at the time of stenting. We have recently reported that the inhibitory potency of DNAzymes in SMCs can be improved by the incorporation of certain structural modifications such as locked nucleic acids (LNA). Ohtani et al demonstrated that intraluminal delivery of double-stranded cis-element oligonucleotide "decoys" bearing Egr-1 binding sites inhibit the expression of Egr-1–dependent genes, such as PDGF-B, TGF-ß, and MCP-1, and block intimal hyperplasia 7 and 28 days, respectively, after balloon injury to the carotid arteries of hypercholesterolemic rabbits. It is presently unknown whether injury-inducible intimal thickening is compromised in Egr-1–null mice. Thus, antisense, DNAzyme and decoy approaches targeting Egr-1, which is rapidly upregulated by acute injury, may be useful as antigene strategies in vascular occlusive disorders. Blockade of neointima formation by targeting other transc**tion factors, such as NFAT, STAT3, nuclear factor  B, and c-Jun, that are also activated by arterial injury, suggests that the possibility of compound inhibition of postangioplasty restenosis in strategies targeting multiple factors.

夜*城

大家 既然都很忙。。我已找其他的网站帮忙翻译了，，上面的帖子宣布作废:(