Impaired regulatory volume decrease in freshly isolated cholangiocytes from cystic fibrosis mice: implications for cystic fibrosis transmembrane conductance regulator effect on potassium conductance.
Impaired regulatory volume decrease in freshly isolated cholangiocytes from cystic fibrosis mice: implications for cystic fibrosis transmembrane conductance regulator effect on potassium conductance.
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囊性纤维化小鼠新鲜分离的胆管细胞的调节体积减少受损：囊性纤维化跨膜电导调节剂对钾电导的影响的影响。
DOI：
10.1074/jbc.m310855200
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发表时间：
2004
期刊：
影响因子：
--
通讯作者：
Zinzow,Wendy
中科院分区：
文献类型：
--
作者：
Cho,WonKyoo;Siegrist,VickiJ;Zinzow,Wendy
Various K+and Cl–channels are important in cell volume regulation and biliary secretion, but the specific role of cystic fibrosis transmembrane conductance regulator in cholangiocyte cell volume regulation is not known. The goal of this research was to study regulatory volume decrease (RVD) in bile duct cell clusters (BDCCs) from normal and cystic fibrosis (CF) mouse livers. Mouse BDCCs without an enclosed lumen were prepared as described (Cho, W. K. (2002)Am. J. Physiol.283, G1320–G1327). The isotonic solution consisted of HEPES buffer with 40% of the NaCl replaced with isomolar amounts of sucrose, whereas hypotonic solution was the same as isotonic solution without sucrose. The cell volume changes were indirectly assessed by measuring cross-sectional area (CSA) changes of the BDCCs using quantitative videomicroscopy. Exposure to hypotonic solutions increased relative CSAs of normal BDCCs to 1.20 ± 0.01 (mean ± S.E.,n= 50) in 10 min, followed by RVD to 1.07 ± 0.01 by 40 min. Hypotonic challenge in CF mouse BDCCs also increased relative CSA to 1.20 ± 0.01 (n= 53) in 10 min but without significant recovery. Coadministration of the K+-selective ionophore valinomycin restored RVD in CF mouse BDCCs, suggesting that the impaired RVD was likely from a defect in K+conductance. Moreover, this valinomycin-induced RVD in CF mice was inhibited by 5-nitro-2′-(3-phenylpropylamino)-benzoate, indicating that it is not from nonspecific effects. Neither cAMP nor calcium agonists could reverse the impaired RVD seen in CF cholangiocytes. Our conclusion is that CF mouse cholangiocytes have defective RVD from an impaired K+efflux pathway, which could not be reversed by cAMP nor calcium agonists.
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