Over expression of stem cell homing cytokines in urogenital organs following vaginal distention.
OBJECTIVE
Vaginal delivery is a risk factor for stress urinary incontinence. Rat models of simulated childbirth demonstrated hypoxia of the urogenital organs as well as the development of stress urinary incontinence following vaginal distention. Stromal derived factor-1 and monocyte chemotactic protein-3 were identified as cytokines that are over expressed after myocardial ischemia and signal stem cell migration to ischemic sites in a rat cardiac model. Given the focal hypoxia observed with vaginal distention, we characterized stromal derived factor-1 and monocyte chemotactic protein-3 expression by pelvic organ tissues after vaginal distention.


METHODS
A total of 16 female rats were randomized into 4 groups. Two groups underwent vaginal distention with harvest of pelvic tissues immediately or 24 hours after vaginal distention, a sham group underwent anesthesia only and a control group underwent no intervention. Reverse transcriptase-polymerase chain reaction was performed on RNA extracted from the urogenital organs.


RESULTS
Monocyte chemotactic protein-3 expression in the urethra was increased 20 and 6-fold immediately and 24 hours after vaginal distention, respectively. Monocyte chemotactic protein-3 was 8 and 4-fold increased in the vagina after vaginal distention. There was no difference in monocyte chemotactic protein-3 expression in the rectum or bladder in any group. Stromal derived factor-1 was significantly under expressed immediately after vaginal distention in all tissues.


CONCLUSIONS
Monocyte chemotactic protein-3 is significantly over expressed in rat urethral and vaginal tissues immediately following vaginal distention with above normal but decreasing expression 24 hours later. The association between monocyte chemotactic protein-3 over expression and targeted stem cell migration is under investigation. Successful characterization and control of such a repair mechanism in the lower urinary tract would introduce the potential for novel nonoperative treatments and/or preventive measures for stress urinary incontinence.
Woo
Lynn L
LL
Glickman Urological Institute, Cleveland Clinic, Cleveland, OH 44120, USA. wool@ccf.org
Hijaz
Adonis
A
Kuang
Mei
M
Penn
Marc S
MS
Damaser
Margot S
MS
Rackley
Raymond R
RR
D000818:Animals; D002465:Cell Movement; D054410:Chemokine CCL7; D054377:Chemokine CXCL12; D019743:Chemokines, CXC / Q000096:biosynthesis*; D005260:Female; D007327:Insufflation; D018945:Monocyte Chemoattractant Proteins; D051381:Rats; D017207:Rats, Sprague-Dawley; D013234:Stem Cells / Q000502:physiology*; D014521:Urethra / Q000378:metabolism*; D001743:Urinary Bladder / Q000378:metabolism*; D014621:Vagina / Q000378:metabolism*
C515452:Ccl7 protein, rat; D054410:Chemokine CCL7; D054377:Chemokine CXCL12; D019743:Chemokines, CXC; D018945:Monocyte Chemoattractant Proteins