1. Gene Therapy for Erectile Dysfunction: Fact or Fiction?
Muammer Kendirci, Patrick E. Teloken, Hunter C. Champion, Wayne J.G. Hellstrom, Trinity J. Bivalacqua 
European Urology 
Volume 50, Issue 6, Pages (December 2006)
DOI: /j.eururo
Copyright © 2006 European Association of Urology Terms and Conditions

2. Fig. 1
Schematic drawing of the principles of gene therapy. Therapeutic genes of interest or growth factors that influence cellular function can be placed in viral or nonviral vectors that enter a targeted cell to significantly alter its function. This figure demonstrates the administration of a desired gene and subsequent transportation into the nucleus and alteration of cellular function. More specific delineation of the mechanisms for vector incorporation of a specific gene into a targeted cell and the alteration in cellular function can be found in the text and reference list.
European Urology  , DOI: ( /j.eururo )
Copyright © 2006 European Association of Urology Terms and Conditions

3. Fig. 2
(A) Potential molecular targets that cause corporal smooth muscle relaxation. Endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor (VEGF) gene therapies increase endothelial-derived NO and promote corporal vasodilation. Additionally, VEGF preserves corporal smooth muscle integrity. Extracellular superoxide dismutase (EC-SOD) gene therapy reduces penile superoxide anion levels thus improving NO bioavailability and corporal smooth muscle relaxation. Neuronal NOS (nNOS) and brain-derived neurotrophic factor (BDNF) gene therapies increase nNOS expression and neuronal-derived NO. Vasoactive intestinal polypeptide (VIP) and calcitonin gene-related peptide (CGRP) gene therapies increase corporal cyclic adenosine monophosphate (cAMP) levels via activation of adenylate cyclase to increase corporal smooth muscle relaxation. Maxi-K channel (Ca2+-sensitive potassium channel) hyperpolarises corporal smooth muscle to promote vasodilation. (B) Inhibition of RhoA or Rho-kinase using dominant-negative mutants promotes myosin light-chain (MLC) phosphatase to an activated form (nonphosphorylated), thus catalysing the dephosphorylation of MLC and thereby increasing corporal smooth muscle relaxation. Ach=acetylcholine; M3=muscarinic receptor; l-arg=l-arginine; NO=nitric oxide; IP3=inositol 1,4,5-trisphosphate; AA=arachidonic acid; PGE2=prostaglandin E2; PG=prostaglandin; GC=guanylate cyclase; AC=adenylate cyclase; PLC=phospholipase C; PKG=protein kinase G; PKA=protein kinase A; ET=endothelin; NE=norepinephrine; EP=prostaglandin receptor.
European Urology  , DOI: ( /j.eururo )
Copyright © 2006 European Association of Urology Terms and Conditions