Suburothelial myofibroblasts in the human overactive bladder and the effect of botulinum neurotoxin type A treatment.
Alexander Roosen,Soumendra N Datta,Rasheda A Chowdhury,Pravina M Patel,Vinay Kalsi,Sohier Elneil,Prokar Dasgupta,Thomas M Kessler,Shahid Khan,Jalesh Panicker,Christopher H Fry,Sebastian Brandner,Clare J Fowler,Apostolos Apostolidis
European urology
55
2009
Mostrar resumen
An increasing body of evidence suggests a possible role of suburothelial myofibroblasts (MFs) in bladder mechanosensation and in the pathophysiology of detrusor overactivity (DO). | | 19054608
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Cadherin-11 up-regulation in overactive bladder suburothelial myofibroblasts.
Alexander Roosen,Apostolos Apostolidis,Sohier Elneil,Shahid Khan,Jalesh Panicker,Sebastian Brandner,Clare J Fowler,Thomas M Kessler
The Journal of urology
182
2009
Mostrar resumen
We investigated whether the adherens junction proteins cadherin-11 and beta-catenin can be immunohistochemically visualized in the human bladder using commercially available antibodies and, if so, whether there are differences between patients with overactive bladder and refractory detrusor overactivity, and controls without lower urinary tract symptoms. | | 19450843
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ADAR2-dependent RNA editing of AMPA receptor subunit GluR2 determines vulnerability of neurons in forebrain ischemia.
Peng, Peter L, et al.
Neuron, 49: 719-33 (2006)
2005
Mostrar resumen
ADAR2 is a nuclear enzyme essential for GluR2 pre-mRNA editing at Q/R site-607, which gates Ca2+ entry through AMPA receptor channels. Here, we show that forebrain ischemia in adult rats selectively reduces expression of ADAR2 enzyme and, hence, disrupts RNA Q/R site editing of GluR2 subunit in vulnerable neurons. Recovery of GluR2 Q/R site editing by expression of exogenous ADAR2b gene or a constitutively active CREB, VP16-CREB, which induces expression of endogenous ADAR2, protects vulnerable neurons in the rat hippocampus from forebrain ischemic insult. Generation of a stable ADAR2 gene silencing by delivering small interfering RNA (siRNA) inhibits GluR2 Q/R site editing, leading to degeneration of ischemia-insensitive neurons. Direct introduction of the Q/R site edited GluR2 gene, GluR2(R607), rescues ADAR2 degeneration. Thus, ADAR2-dependent GluR2 Q/R site editing determines vulnerability of neurons in the rat hippocampus to forebrain ischemia. | Rat | 16504947
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Urologic applications of botulinum toxin therapy for voiding dysfunction.
Raymond Rackley,Joseph Abdelmalak
Current urology reports
5
2004
Mostrar resumen
Botulinum toxin is primarily a presynaptic neuromuscular blocking agent inducing selective and reversible muscle weakness up to several months when injected intramuscularly in small quantities. The clinical use of botulinum toxin type-A has gained widespread acceptance and application for numerous adult and pediatric spasticity syndromes. This has led to the urologic adoption of this minimally invasive therapy for the treatment of idiopathic and neurogenic detrusor overactivity, interstitial cystitis, detrusor-sphincter dyssynergia, urinary retention, and prostatic conditions. Outlined below is an overview of the clinical adoption of this therapy for the treatment of various dysfunctions of the lower urinary tract. | | 15461917
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