Department of Biomedical Engineering, Cleveland Clinic, Cleveland, Ohio 44195, USA.
J Urol. 2013 Apr;189(4):1588-94. doi: 10.1016/j.juro.2012.09.096. Epub 2012 Sep 25.
Human childbirth simulated by vaginal distention is known to increase the expression of chemokines and receptors involved in stem cell homing and tissue repair. We hypothesized that pregnancy and parturition in rats contributes to the expression of chemokines and receptors after vaginal distention.
We used 72 age matched female Lewis rats, including virgin rats with and without vaginal distention, and delivered rats with and without vaginal distention. Each rat was sacrificed immediately, or 3 or 7 days after vaginal distention and/or parturition, and the urethra was harvested. Relative expression of chemokines and receptors was determined by real-time polymerase chain reaction. Mixed models were used with the Bonferroni correction for multiple comparisons.
Vaginal distention up-regulated urethral expression of CCL7 immediately after injury in virgin and postpartum rats. Hypoxia inducible factor-1α and vascular endothelial growth factor were up-regulated only in virgin rats immediately after vaginal distention. CD191 expression was immediately up-regulated in postpartum rats without vaginal distention compared to virgin rats without vaginal distention. CD195 was up-regulated in virgin rats 3 days after vaginal distention compared to virgin rats without vaginal distention. CD193 and CXCR4 showed delayed up-regulation in virgin rats 7 days after vaginal distention. CXCL12 was up-regulated in virgin rats 3 days after vaginal distention compared to immediately after vaginal distention. Interleukin-8 and CD192 showed no differential expression.
Vaginal distention results in up-regulation of the chemokines and receptors expressed during tissue injury, which may facilitate the spontaneous functional recovery previously noted. Pregnancy and delivery up-regulated CD191 and attenuated the expression of hypoxia inducible factor-1α and vascular endothelial growth factor in the setting of vaginal distention, likely by decreasing hypoxia.
阴道扩张模拟人类分娩已知会增加参与干细胞归巢和组织修复的趋化因子和受体的表达。我们假设大鼠妊娠和分娩有助于阴道扩张后趋化因子和受体的表达。
我们使用了 72 只年龄匹配的雌性 Lewis 大鼠，包括有和没有阴道扩张的处女大鼠，以及有和没有阴道扩张的分娩大鼠。每只大鼠在阴道扩张和/或分娩后立即或 3 或 7 天被处死，采集尿道。通过实时聚合酶链反应测定趋化因子和受体的相对表达。使用混合模型和 Bonferroni 校正进行多重比较。
阴道扩张在处女和产后大鼠损伤后立即上调尿道中 CCL7 的表达。缺氧诱导因子-1α 和血管内皮生长因子仅在处女大鼠阴道扩张后立即上调。与无阴道扩张的处女大鼠相比，无阴道扩张的产后大鼠的 CD191 表达立即上调。与无阴道扩张的处女大鼠相比，阴道扩张后 3 天的处女大鼠 CD195 上调。阴道扩张后 7 天的处女大鼠 CD193 和 CXCR4 表现出延迟上调。与阴道扩张后立即相比，阴道扩张后 3 天的处女大鼠 CXCL12 上调。白细胞介素-8 和 CD192 没有差异表达。
阴道扩张导致组织损伤期间表达的趋化因子和受体上调，这可能有助于先前观察到的自发功能恢复。妊娠和分娩上调 CD191，并在阴道扩张的情况下减弱缺氧诱导因子-1α 和血管内皮生长因子的表达，可能通过降低缺氧来实现。
