ArticleGene therapy2009
Herpes simplex virus vector-mediated gene delivery of glutamic acid decarboxylase reduces detrusor overactivity in spinal cord-injured rats.
Article in Gene therapy, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 43 citations in OpenAlex.
- Non-replicative herpes simplex virus genomic and amplicon vectors for gene therapy - an update.Gene therapy · 2025Review
- Molecular Mechanisms of Neurogenic Lower Urinary Tract Dysfunction after Spinal Cord Injury.International journal of molecular sciences · 2023Review
- Viral Vector-Mediated Gene Transfer of Glutamic Acid Decarboxylase for Chronic Pain Treatment: A Literature Review.Human gene therapy · 2020Review
- Article
- New Frontiers of Basic Science Research in Neurogenic Lower Urinary Tract Dysfunction.The Urologic clinics of North America · 2017Review
- Article
- HSV vector-mediated GAD67 suppresses neuropathic pain induced by perineural HIV gp120 in rats through inhibition of ROS and Wnt5a.Gene therapy · 2016Article
- The role of brain-derived neurotrophic factor (BDNF) in the development of neurogenic detrusor overactivity (NDO).The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Neural control of the lower urinary tract.Comprehensive Physiology · 2015Review
- Intravesical TRPV4 blockade reduces repeated variate stress-induced bladder dysfunction by increasing bladder capacity and decreasing voiding frequency in male rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Article
- Herpes simplex virus vector-mediated gene transfer of kynurenine aminotransferase improves detrusor overactivity in spinal cord-injured rats.Gene therapy · 2014Article
- Neural mechanisms underlying lower urinary tract dysfunction.Korean journal of urology · 2014Review
- Treatment of overactive bladder: what is on the horizon?International urogynecology journal · 2013Review
- Gene therapy for the treatment of chronic peripheral nervous system pain.Neurobiology of disease · 2012Review
- Plasticity in reflex pathways to the lower urinary tract following spinal cord injury.Experimental neurology · 2012Review
- Cellular therapies for treating pain associated with spinal cord injury.Journal of translational medicine · 2012Review
- Suppression of detrusor-sphincter dyssynergia by herpes simplex virus vector mediated gene delivery of glutamic acid decarboxylase in spinal cord injured rats.The Journal of urology · 2010Article
- Changes in afferent activity after spinal cord injury.Neurourology and urodynamics · 2010Review
- Roles of Glycinergic and Gamma-aminobutyric-ergic Mechanisms in the Micturition Reflex in Rats.Lower urinary tract symptoms · 2009Article
- Current Knowledge and Novel Frontiers in Lower Urinary Tract Dysfunction after Spinal Cord Injury: Basic Research Perspectives.Urological scienceArticle
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
We examined whether replication-defective herpes simplex virus (HSV) vectors encoding the 67 kDa form of the glutamic acid decarboxylase (GAD(67)) gene product, the gamma-aminobutyric acid (GABA) synthesis enzyme, can suppress detrusor overactivity (DO) in rats with spinal cord injury (SCI). One week after spinalization, HSV vectors expressing GAD and green fluorescent protein (GFP) (HSV-GAD) were injected into the bladder wall. Rats with SCI without HSV injection (HSV-untreated) and those injected with lacZ-encoding reporter gene HSV vectors (HSV-LacZ) were used as controls. Three weeks after viral injection, continuous cystometry was performed under awake conditions in all three groups. In the HSV-GAD group, the number and amplitude of non-voiding contractions (NVCs) were significantly decreased (40-45% and 38-40%, respectively) along with an increase in voiding efficiency, compared with HSV-untreated and HSV-LacZ groups, but micturition pressure was not different among the three groups. Intrathecal application of bicuculline partly reversed the decreased number and amplitude of NVCs, and decreased voiding efficiency in the HSV-GAD group. In the HSV-GAD group, GAD(67) mRNA and protein levels were significantly increased in the L6-S1 dorsal root ganglia (DRG) compared with the HSV-LacZ group, while 57% of DRG cells were GFP-positive, and these neurons showed increased GAD(67)-like immunoreactivity compared with the HSV-LacZ group. These results indicate that GAD gene therapy effectively suppresses DO after SCI predominantly through the activation of spinal GABA(A) receptors. Thus, HSV-based GAD gene transfer to bladder afferent pathways may represent a novel approach for treatment of neurogenic DO.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.