Changes in detrusor smooth muscle myosin heavy chain mRNA expression following spinal cord injury in the mouse
✍ Scribed by Tracey S. Wilson; Khaled Abdel Aziz; Dolores Vazques; Lisa-Ann Wuermser; Victor K. Lin; Gary E. Lemack
- Publisher
- John Wiley and Sons
- Year
- 2005
- Tongue
- English
- Weight
- 277 KB
- Volume
- 24
- Category
- Article
- ISSN
- 0733-2467
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Aims
Smooth muscle myosin heavy chain (SMMHC) isoform composition has been shown to be developmentally regulated and to be associated with functional changes in smooth muscle activity. In this study, we sought to determine expression patterns of SMMHC isoforms in a murine model of spinal cord injury (SCI) and to compare these expression patterns to neurologic, cytometric, and morphometric findings.
Materials and Methods
Baseline cystometry was performed on adult, female mice followed by either thoracic spinal cord transection (SCI) or sham operation (Sham). At 1, 3, or 6 weeks postoperatively neurologic evaluation and cystometry were performed, bladders were harvested, and expression patterns of SMMHC isoforms (SM1 vs. SM2 and SMA vs. SMB) were assessed by RT‐PCR. Morphometrics utilizing computer‐assisted color image analysis was also performed on all bladders.
Results
There was a significant increase in bladder weight and capacity 1 week following SCI which normalized over time, however, morphometric analysis did not reveal an alteration in tissue composition amongst the three groups. One week following SCI, SM1 was predominantly expressed over SM2 and began to normalize at 3 weeks. This coincided with the emergence of reflex voiding and detrusor overactivity. SMA was expressed following SCI only, and the number of bladders found to express SMA decreased with increasing duration since SCI.
Conclusions
Smooth muscle myosin heavy chain mRNA expression patterns appear to be affected by SCI. We believe the induction of SMA may be a factor in altered bladder function following injury. © 2004 Wiley‐Liss, Inc.