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首页> 外文期刊>Journal of Cellular Physiology >Nitric oxide regulation of Na, K-ATPase activity in ocular ciliary epithelium involves Src family kinase
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Nitric oxide regulation of Na, K-ATPase activity in ocular ciliary epithelium involves Src family kinase

机译：一氧化氮调控Na, K-ATPase活动在眼睫状上皮包括Src的家庭激酶

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摘要

The nitric oxide (NO) donor sodium nitroprusside (SNP) is known to reduce aqueous humor (AH) secretion in the isolated porcine eye. Previously, SNP was found to inhibit Na,K-ATPase activity in nonpigmented ciliary epithelium (NPE), AH-secreting cells, through a cGMP/protein kinase G (PKG)-mediated pathway. Here we show Src family kinase (SFK) activation in the Na,K-ATPase activity response to SNP. Ouabain-sensitive 86Rb uptake was reduced by 35% in cultured NPE cells exposed to SNP (100μM) or exogenously added cGMP (8-Br-cGMP) (100μM) and the SFK inhibitor PP2 (10μM) prevented the response. Ouabain-sensitive ATP hydrolysis was reduced by ～40% in samples detected in material obtained from SNP- and 8-Br-cGMP-treated cells following homogenization, pointing to an intrinsic change of Na,K-ATPase activity. Tyrosine-10 phosphorylation of Na,K-ATPase α1 subunit was detected in SNP and L-arginine-treated cells and the response prevented by PP2. SNP elicited an increase in cell cGMP. Cells exposed to 8-Br-cGMP displayed SFK activation (phosphorylation) and inhibition of both ouabain-sensitive 86Rb uptake and Na,K-ATPase activity that was prevented by PP2. SFK activation, which also occurred in SNP-treated cells, was suppressed by inhibitors of soluble guanylate cyclase (ODQ; 10μM) and PKG (KT5823; 1μM). SNP and 8-Br-cGMP also increased phosphorylation of ERK1/2 and p38 MAPK and the response prevented by PP2. However, U0126 did not prevent SNP or 8-Br-cGMP-induced inhibition of Na,K-ATPase activity. Taken together, the results suggest that NO activates guanylate cyclase to cause a rise in cGMP and subsequent PKG-dependent SFK activation. Inhibition of Na,K-ATPase activity depends on SFK activation.
机译：一氧化氮(NO)供体硝普酸钠(SNP)是减少房水(啊)孤立的猪眼分泌物。以前,SNP发现抑制Na, K-ATPase活动nonpigmented纤毛上皮(肺水肿)AH-secreting细胞,通过cGMP /蛋白质激酶G (PKG)介导的通路。家族激酶(SFK)激活Na, K-ATPase活动对SNP。吸收降低了在培养肺水肿的35%细胞暴露于SNP(100μM)或体内补充道cGMP (8-Br-cGMP)(100μM)和SFK抑制剂PP2(10μM)阻止了反应。Ouabain-sensitive ATP水解减少了~ 40%样本中检测到的材料SNP -和8-Br-cGMP-treated细胞均质化,指着一个内在变化Na, K-ATPase活动。Na的磷酸化,K-ATPaseα1亚基检测SNP和L-arginine-treated细胞响应由PP2阻止。增加细胞环鸟苷酸。SFK激活(磷酸化)和显示抑制ouabain-sensitive 86 rb吸收预防和Na, K-ATPase活动PP2。SNP-treated细胞,抑制了抑制剂可溶性鸟苷酸环化酶(ODQ;(KT5823;ERK1/2和p38 MAPK的磷酸化由PP2反应阻止了。防止SNP或8-Br-cGMP-induced抑制Na, K-ATPase活动。建议没有激活鸟苷酸环化酶导致cGMP上升和随后PKG-dependentSFK激活。活动取决于SFK激活。

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