Aims: To determine the role of p75 neurotrophin receptor (p75 ) and the therapeutic effect of the selective small molecule p75 modulator, LM11A-31, in spinal cord injury (SCI) induced lower urinary tract dysfunction (LTUD) using a mouse model.
Methods: Adult female T -T transected mice were gavaged daily with LM11A-31 (100 mg/kg) for up to 6 weeks, starting 1 day before, or 7 days following injury. Mice were evaluated in vivo using urine spot analysis, cystometrograms (CMGs), and external urethral sphincter (EUS) electromyograms (EMGs); and in vitro using histology, immunohistochemistry, and Western blot.
Results: Our studies confirm highest expression of p75 in the detrusor layer of the mouse bladder and lamina II region of the dorsal horn of the lumbar-sacral (L -S ) spinal cord which significantly decreased following SCI. LM11A-31 prevented or ameliorated the detrusor sphincter dyssynergia (DSD) and detrusor overactivity (DO) in SCI mice, significantly improving bladder compliance. Furthermore, LM11A-31 treatment blocked the SCI-related urothelial damage and bladder wall remodeling.
Conclusion: Drugs targeting p75 can moderate DSD and DO in SCI mice, may identify pathophysiological mechanisms, and have therapeutic potential in SCI patients.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6202156 | PMC |
| http://dx.doi.org/10.1002/nau.23722 | DOI Listing |
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