Department of Pediatrics-0830, School of Medicine, University of California-San Diego, La Jolla, CA 92093-0830, USA.
J Physiol. 2010 Jul 1;588(Pt 13):2329-42. doi: 10.1113/jphysiol.2010.187237. Epub 2010 May 17.
Cervical mucus thinning and release during the female reproductive cycle is thought to rely mainly on fluid secretion. However, we now find that mucus released from the murine reproductive tract critically depends upon concurrent bicarbonate (HCO(3)(-)) secretion. Prostaglandin E(2) (PGE(2))- and carbachol-stimulated mucus release was severely inhibited in the absence of serosal HCO(3)(-), HCO(3)(-) transport, or functional cystic fibrosis transmembrane conductance regulator (CFTR). In contrast to mucus release, PGE(2)- and carbachol-stimulated fluid secretion was not dependent on bicarbonate or on CFTR, but was completely blocked by niflumic acid. We found stimulated mucus release was severely impaired in the cystic fibrosis F508 reproductive tract, even though stimulated fluid secretion was preserved. Thus, CFTR mutations and/or poor bicarbonate secretion may be associated with reduced female fertility associated with abnormal mucus and specifically, may account for the increased viscosity and lack of cyclical changes in cervical mucus long noted in women with cystic fibrosis.
在女性生殖周期中，宫颈黏液变薄和排出被认为主要依赖于液体分泌。然而，我们现在发现，从鼠类生殖道排出的黏液严重依赖于同时的碳酸氢盐（HCO（3）（-））分泌。在没有腹膜 HCO（3）（-）、HCO（3）（-）转运或功能性囊性纤维化跨膜电导调节因子（CFTR）的情况下，前列腺素 E（2）（PGE（2））和卡巴胆碱刺激的黏液释放受到严重抑制。与黏液释放不同，PGE（2）和卡巴胆碱刺激的液体分泌不依赖于碳酸氢盐或 CFTR，但完全被尼氟酸阻断。我们发现，即使刺激的液体分泌得到保留，囊性纤维化 F508 生殖道中的 PGE（2）和卡巴胆碱刺激的黏液释放也严重受损。因此，CFTR 突变和/或碳酸氢盐分泌不良可能与异常黏液相关的女性生育能力降低有关，特别是可能解释了囊性纤维化女性中宫颈黏液长期以来观察到的增加的粘度和缺乏周期性变化。
