Center for Systems Biology/Program in Membrane Biology/Nephrology Division, Massachusetts General Hospital, Boston, Massachusetts; and.
Am J Physiol Cell Physiol. 2013 Aug 15;305(4):C436-46. doi: 10.1152/ajpcell.00410.2012. Epub 2013 Jun 12.
Clear cells express the vacuolar proton-pumping H(+)-ATPase (V-ATPase) and acidify the lumen of the epididymis, a process that is essential for male fertility. The renin-angiotensin-aldosterone system (RAAS) regulates fluid and electrolyte balance in the epididymis, and a previous study showed binding of aldosterone exclusively to epididymal clear cells (Hinton BT, Keefer DA. Steroid Biochem 23: 231-233, 1985). We examined here the role of aldosterone in the regulation of V-ATPase in the epididymis. RT-PCR showed expression of the mineralocorticoid receptor [MR; nuclear receptor subfamily 3, group C member 2 (NR3C2)] and 11-β-dehydrogenase isozyme 2 (HSD11β2) mRNAs specifically in clear cells, isolated by fluorescence-activated cell sorting from B1-enhanced green fluorescent protein (EGFP) mice. Tail vein injection of adult rats with aldosterone, 1,2-dioctanoyl-sn-glycerol (DOG), or 8-(4-chlorophenylthio)-cAMP (cpt-cAMP) induced V-ATPase apical membrane accumulation and extension of V-ATPase-labeled microvilli in clear cells in the caput epididymis but not in the cauda. V-ATPase activity was measured in EGFP-expressing clear cells using the intracellular pH (pHi)-sensing dye seminaphthorhodafluor-5F-5-(and 6)-carboxylic acid, acetoxymethyl ester acetate (SNARF-5F). Aldosterone induced a rapid increase in the rate of Na(+)- and bicarbonate-independent pHi recovery following an NH4Cl-induced acid load in clear cells isolated from the caput but not the cauda. This effect was abolished by concanamycin A, spironolactone, and chelerythrine but not myristoylated-protein kinase inhibitor (mPKI) or mifepristone. Thus aldosterone increases V-ATPase-dependent proton secretion in clear cells in the caput epididymis via MR/NR3C2 and PKC activation. This study, therefore, identifies aldosterone as an active member of the RAAS for the regulation of luminal acidification in the proximal epididymis.
透明细胞表达液泡质子泵 H(+)-ATP 酶 (V-ATPase),并使附睾管腔酸化,这一过程对男性生育能力至关重要。肾素-血管紧张素-醛固酮系统 (RAAS) 调节附睾中的液体和电解质平衡,先前的一项研究表明醛固酮仅与附睾透明细胞结合 (Hinton BT, Keefer DA. Steroid Biochem 23: 231-233, 1985)。我们在此研究了醛固酮在调节附睾 V-ATPase 中的作用。RT-PCR 显示,核受体亚家族 3 组 C 成员 2 (NR3C2) 和 11-β-脱氢酶同工酶 2 (HSD11β2) mRNA 仅在通过荧光激活细胞分选从 B1 增强型绿色荧光蛋白 (EGFP) 小鼠中分离的透明细胞中表达。醛固酮、1,2-二油酰基-sn-甘油 (DOG) 或 8-(4-氯苯基硫代)-cAMP (cpt-cAMP) 尾静脉注射成年大鼠诱导 V-ATPase 顶端膜积累,并使透明细胞中 V-ATPase 标记的微绒毛延伸在附睾头部,但不在尾部。在 EGFP 表达的透明细胞中,使用细胞内 pH (pHi) 感应染料 seminaphthorhodafluor-5F-5-(和 6)-羧酸,乙酰氧甲酯乙脂 (SNARF-5F) 测量 V-ATPase 活性。醛固酮诱导从头部分离的透明细胞中 NH4Cl 诱导的酸负荷后,Na(+)-和碳酸氢盐非依赖性 pHi 恢复的速率迅速增加,但从尾部分离的透明细胞中没有。该作用被康纳霉素 A、螺内酯和 Chelerythrine 但不是豆蔻酰化蛋白激酶抑制剂 (mPKI) 或米非司酮所消除。因此,醛固酮通过 MR/NR3C2 和 PKC 激活增加透明细胞中 V-ATPase 依赖性质子分泌,从而在附睾头部增加质子分泌。因此,这项研究确定醛固酮是 RAAS 的一个活跃成员,用于调节近侧附睾管腔酸化。