Expression of ENaC subunits, chloride channels, and aquaporins in ovine fetal lung: ontogeny of expression and effects of altered fetal cortisol concentrations.
Expression of ENaC subunits, chloride channels, and aquaporins in ovine fetal lung: ontogeny of expression and effects of altered fetal cortisol concentrations.
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ENaC 亚基、氯离子通道和水通道蛋白在绵羊胎肺中的表达：表达的个体发育和胎儿皮质醇浓度改变的影响。
DOI：
10.1152/ajpregu.00127.2009
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发表时间：
2009
期刊：
影响因子：
--
通讯作者：
Keller-Wood,Maureen
中科院分区：
文献类型：
--
作者：
Jesse,NathanM;McCartney,Jarret;Feng,Xiaodi;Richards,ElaineM;Wood,CharlesE;Keller-Wood,Maureen
Transition of the epithelium of the fetal lung from fluid secretion to fluid reabsorption requires changes in the expression of ion channels. Corticosteroids regulate expression of several of these channels, including the epithelium sodium channel (ENaC) subunits and aquaporins (AQP). We investigated the ontogenetic changes in these ion channels in the ovine fetal lung during the last half of gestation, a time of increasing adrenal maturation. Expression of the mRNAs for the chloride channels, cystic fibrosis transmembrane conductance regulator (CFTR), and chloride channel 2 (CLCN2) decreased with age. Expression of mRNAs for AQP1, AQP5, and for subunits of ENaC (α, β, γ) increased with age. In the fetal sheep the expression of ENaCβ mRNA was dramatically higher than the expression of ENaCα or ENaCγ, but expression of ENaCβ protein decreased with maturation, although the ratio of the mature (112 kDa) to immature (102 kDa) ENaCβ protein increased with age, particularly in the membrane fraction. In contrast, ENaCα mRNA and protein both increase with maturation, and the mature form of ENaCα (68 kDa) predominates at all ages. A modest increase in fetal cortisol, within the range expected to occur naturally in late gestation but prior to active labor, increased ENaCα mRNA but not ENaCβ, ENaCγ, or AQP mRNAs. We conclude that in the ovine fetal lung, appearance of functional sodium channels is associated with induction of ENACα and ENaCγ, and that ENaCα expression may be induced by even small, preterm increases in fetal cortisol.
