Smooth muscle myosin heavy chain and caldesmon expression in the anterior vaginal wall of women with and without pelvic organ prolapse

Objective: The aim of this study was to quantify the expression of smooth muscle myosin heavy chain (SM-MHC) and caldesmon in the anterior vaginal wall of women with and without pelvic organ prolapse. Study Design: Immunoblot analysis was conducted on protein extracts from the vaginal muscularis of...

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Veröffentlicht in:American journal of obstetrics and gynecology 2001-10, Vol.185 (4), p.944-952
Hauptverfasser: Boreham, Muriel K., Miller, Rodney T., Schaffer, Joseph I., Word, R.Ann
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Sprache:eng
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Zusammenfassung:Objective: The aim of this study was to quantify the expression of smooth muscle myosin heavy chain (SM-MHC) and caldesmon in the anterior vaginal wall of women with and without pelvic organ prolapse. Study Design: Immunoblot analysis was conducted on protein extracts from the vaginal muscularis of 15 women with and 11 women without pelvic organ prolapse by using specific antibodies for SM-MHC, nonmuscle MHC-B, and caldesmon. The fraction of muscularis containing smooth muscle was determined by morphometric analysis of histologic cross sections. Reverse transcriptase–polymerase chain reaction was used to amplify SM-MHC isoforms produced by alternative splicing in the myosin head. Results: Whereas the expression of SM-MHC was increased modestly (2-fold), expression of smooth muscle caldesmon was increased 6- to 7-fold in vaginal muscularis from women with prolapse. The relative distribution of SM-MHC isoforms was similar in both groups. Conclusions: Caldesmon is increased substantially in vaginal smooth muscle of women with pelvic organ prolapse. Caldesmon inhibits actin-activated myosin magnesium adenosine triphosphatase activity and inhibits the maintenance of contractile force. Thus, this disproportionate increase in caldesmon, relative to myosin, may result in inhibition of vaginal smooth muscle contractility and force maintenance. (Am J Obstet Gynecol 2001;185: 944-52.)
ISSN:0002-9378
1097-6868
DOI:10.1067/mob.2001.117342