Co action of CFTR and AQP1 increases permeability of peritoneal epithelial cells on estrogen-induced ovarian hyper stimulation syndrome

Yong-Chao Lu,Qin-Fu Han,Ling Li,Pei-Yin Jin

doi:10.1186/1471-2121-13-23

Abstract

BackgroundOvarian hyper stimulation syndrome (OHSS) is an iatrogenic complication associated with fertility drugs. It is characterized by increased vascular permeability and substantial fluid shift with accumulation in the body cavity. The pathogenesis of OHSS remains obscure, and no definitive treatments are currently available.ResultsUsing western blot and short-circuit current (Isc) techniques, we investigate the potential coactions of analysis in cystic fibrosis transmembrane conductance regulator (CFTR) and aquaporin 1 (AQP1) on the hyper permeability of body cavity peritoneal epithelial cells in the pathogenesis of OHSS. The rats develop OHSS symptoms, with the up regulation of both CFTR and AQP1 expression and enhanced CFTR channel activity in peritoneal epithelial cells, can also be mimicked by administration of estrogen, alone in ovariectomized rats. Administration of progesterone suppresses CFTR activity, OHSS symptoms as well as CFTR and AQP1 expression. Besides, AQP1 inhibitor, HgCl2, can suppress CFTR channel activity. Therefore, antisera against CFTR or AQP1 to OHSS animals may result in alleviation of the symptom.ConclusionThis study confirms the coactions of CFTR and AQP1 play a critical role in the development and progression of increased peritoneal epithelial permeability in severe OHSS. These findings may provide grounds for ameliorating assisted reproduction treatment strategy to reduce the risk of OHSS in in vitro fertilization (IVF).

Highlights

Ovarian hyper stimulation syndrome (OHSS) is an iatrogenic complication associated with fertility drugs
Coaction of the peritoneal epithelial CFTR and aquaporin 1 (AQP1) channel activity in the development of OHSS We found that AQP1 inhibitor (HgCl2) could suppress the CFTR activity in the freshly isolated peritoneal epithelial cells of OHSS rats by the short circuit current (Isc) measurement
Enhancement of aquaporin channel activity [31] and suppression of epithelial sodium channel-mediated absorptive activity [32] that results in net increases in electrolyte and fluid secretion may contribute to the pathogenesis of OHSS

Summary

Introduction

Ovarian hyper stimulation syndrome (OHSS) is an iatrogenic complication associated with fertility drugs It is characterized by increased vascular permeability and substantial fluid shift with accumulation in the body cavity. OHSS is characterized by massive cystic enlargement of the ovaries associated with third space fluid shift This can result in the formation of ascites and pleural effusion in severe conditions due to increased peritoneal epithelial permeability [2]. Rapid passage of fluid into luminal spaces, as seen in OHSS, may be a consequence of abnormal ion transport across the epithelial cells Several pathological conditions, such as cholera-induced diarrhea, in which there is massive fluid efflux of ion and water across epithelial membranes, are mediated by altered expression and function of transepithelial ion channels, cystic fibrosis transmembrane conductance regulator (CFTR) [9]. The coactions of ion channels and AQP1 such as CFTR [12] are important in the process of fluid effusion

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