Nitric oxide-induced signalling in rat lacrimal acinar cells.
Nitric oxide-induced signalling in rat lacrimal acinar cells.
复制标题
一氧化氮诱导大鼠泪腺腺泡细胞中的信号传导。
DOI：
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发表时间：
2002
期刊：
影响因子：
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通讯作者：
S. Dissing
中科院分区：
文献类型：
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作者：
D. Looms;K. Tritsaris;S. Dissing
本研究旨在探讨一氧化氮（NO）在大鼠泪腺泡细胞分泌过程中的生理作用。此外，我们想确定是否腺泡细胞具有内源性一氧化氮合酶（NOS）的活性，通过测量NO的生产使用荧光NO指示剂4，5-二氨基荧光素（NOS-2）。我们通过NO供体S-亚硝基-N-乙酰基-青霉胺（SNAP）从外部来源添加NO来启动研究。用放射免疫测定法（RIA）测定了细胞内环鸟苷5 ′-磷酸（cGMP）（[cGMP]）的浓度，发现SNAP可使[cGMP]迅速增加，达到静息细胞[cGMP]的350%。此外，添加SNAP和升高fura-2负载的泪腺泡细胞中的[cGMP]，导致cGMP依赖性蛋白激酶介导的Ca 2+从细胞内储存中释放，导致细胞内游离Ca 2+浓度（[Ca 2 +]i）升高。Mn 2+猝灭研究表明，Ca 2+释放不伴随Ca 2+内流。最后，我们证明，泪腺泡细胞具有内源性NOS活性，这是激活β-肾上腺素能刺激，而不是单独的上升[Ca 2 +]i。我们发现，在大鼠泪腺泡细胞中，NO和cGMP通过G激酶激活诱导细胞内钙释放。然而，[Ca 2 +]i的变化相对较小，表明该途径在Ca 2+信号传导中起调节作用，因此本身不会引起[Ca 2 +]i的快速瞬时增加。此外，我们认为，内源性产生的NO激活β-肾上腺素能受体刺激，在信号传导到周围组织中起着重要的作用。
The aim of the present study was to investigate the physiological role of nitric oxide (NO) in mediating secretory processes in rat lacrimal acinar cells. In addition, we wanted to determine whether the acinar cells possess endogenous nitric oxide synthase (NOS) activity by measuring NO production using the fluorescent NO indicator 4,5-diaminofluorescein (DAF-2). We initiated investigations by adding NO from an external source by means of the NO-donor, S-nitroso-N-acetyl-penicillamine (SNAP). Cellular concentrations of cyclic guanosine 5'-phosphate (cGMP) ([cGMP]) were measured by radioimmunoassay (RIA), and we found that SNAP induced a fast increase in the [cGMP], amounting to 350% of the [cGMP] in resting cells. Moreover, addition of SNAP and elevating [cGMP] in fura-2 loaded lacrimal acinar cells, resulted in a cGMP-dependent protein kinase-mediated release of Ca2+ from intracellular stores, leading to a rise in the intracellular free Ca2+ concentration ([Ca2+]i). The Mn2+ quenching studies revealed that the Ca2+ release was not accompanied by Ca2+ influx. Finally, we demonstrate that lacrimal acinar cells possess endogenous NOS activity, which is activated by beta-adrenergic stimulation and not by a rise in [Ca2+]i alone. We show that in rat lacrimal acinar cells, NO and cGMP induce Ca2+ release from intracellular stores via G kinase activation. However, the changes in [Ca2+]i are relatively small, suggesting that this pathway plays a modulatory role in Ca2+ signalling, thus not by itself causing fast transient increases in [Ca2+]i. In addition, we suggest that endogenously produced NO activated by beta-adrenergic receptor stimulation, plays an important role in signalling to the surrounding tissue.
NO、血管扩张剂前列腺素和腺苷对骨骼肌血管生成生长因子基因表达的影响。
DOI：
10.1152/jappl.1999.86.5.1513
发表时间：
1999
期刊：
Journal of applied physiology (Bethesda, Md. : 1985)
影响因子：
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作者：
Benoit,H;Jordan,M;Wagner,H;Wagner,PD
通讯作者：
Wagner,PD