ArticleGene therapy2014
Herpes simplex virus vector-mediated gene transfer of kynurenine aminotransferase improves detrusor overactivity in spinal cord-injured rats.
Article in Gene therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Durable tissue-specific transgene expression in newborn mice following intraperitoneal delivery of non-cytotoxic HSV vectors.Molecular therapy. Methods & clinical development · 2025Article
- Non-replicative herpes simplex virus genomic and amplicon vectors for gene therapy - an update.Gene therapy · 2025Review
- Botulinum toxin A improves neurogenic bladder fibrosis by suppressing transforming growth factor β1 expression in rats.Translational andrology and urology · 2021Article
- Inhibiting the kynurenine pathway in spinal cord injury: Multiple therapeutic potentials?Neural regeneration research · 2018Review
- Increasing bladder capacity by foot stimulation in rats with spinal cord injuries.BMC urology · 2017Article
- Article
- Evaluation and Management of Neurogenic Bladder: What Is New in China?International journal of molecular sciences · 2015Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Detrusor overactivity threatens the renal function of patients with spinal cord injury. Suppressing N-methyl-D-aspartate receptors is known to improve detrusor overactivity in rats with spinal cord injury, whereas kynurenic acid, the endogenous antagonist of N-methyl-D-aspartate receptors, is irreversibly synthesized by kynurenine aminotransferases (KATs). In this study, we investigated whether replication-defective herpes simplex virus vector-mediated gene transfer of human KAT II could treat detrusor overactivity by injecting the vectors into the rat bladder wall 1 week after spinal cord injury. Three weeks after injection, we evaluated the cystometry and gene expression of KAT II in L6-S1 dorsal root ganglia. The results showed that the vectors are transported to L6-S1 dorsal root ganglia and upregulate the expression of KAT II, and that they also improve the detrusor overactivity and voiding efficiency. We also proved that N-methyl-D-aspartate receptors were blocked by kynurenic acid in the extracellular solution or the vector-mediated gene transfer of KAT II in cultured rat neurons of L6-S1 dorsal root ganglia by whole-cell patch clamp to explore the mechanisms of gene therapy. Therefore, replication-defective herpes simplex virus vector-mediated KAT II inhibits detrusor overactivity in spinal cord-injured rats, possibly by suppressing N-methyl-D-aspartate receptors in bladder afferent pathways.
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