共查询到20条相似文献,搜索用时 93 毫秒
1.
E. Hara P.S. Reinach Q. Wen P. Iserovich J. Fischbarg 《The Journal of membrane biology》1999,171(1):75-85
We have studied regulatory volume responses of cultured bovine corneal endothelial cells (CBCEC) using light scattering.
We assessed the contributions of fluoxetine (Prozac) and bumetanide-sensitive membrane ion transport pathways to such responses
by determining K+ efflux and influx. Cells swollen by a 20% hypo-osmotic solution underwent a regulatory volume decrease (RVD) response, which
after 6 min restored relative cell volume by 98%. Fluoxetine inhibited RVD recovery; 20 μm by 26%, and 50 μm totally. Fluoxetine had a triphasic effect on K+ efflux; from 20 to 100 μm it inhibited efflux 2-fold, whereas at higher concentrations the efflux first increased to 1.5-fold above the control value,
and then decreased again. Cells shrunk by a 20% hyperosmotic solution underwent a regulatory volume increase (RVI) which also
after 6 min restored the cell volume by 99%. Fluoxetine inhibited RVI; 20 μm by 25%, and 50 μm completely. Bumetanide (1 μm) inhibited RVI by 43%. In a Cl−-free medium, fluoxetine (50–500 μm) progressively inhibited bumetanide-insensitive K+ influx. The inhibitions of RVI and K+ influx induced by fluoxetine 20 to 50 μm were similar to those induced by 1 μm bumetanide and by Cl−-free medium. A computer simulation suggests that fluoxetine can interact with the selectivity filter of K+ channels. The data suggest that CBCEC can mediate RVD and RVI in part through increases in K+ efflux and Na-K-2Cl cotransport (NKCC) activity. Interestingly, the data also suggest that fluoxetine at 20 to 50 μm inhibits NKCC, and at 100–1000 μm inhibits the Na+ pump. One possible explanation for these findings is that fluoxetine could interact with K+-selective sites in K+ channels, the NKC cotransporter and the Na+ pump. 相似文献
2.
3.
4.
5.
6.
7.
8.
Matthias Schaefer 《Basic and Applied Ecology》2009,10(6):582
9.
10.
11.
12.
13.
用原位杂交和免疫组织化学方法研究了基质金属蛋白酶MMP-2, -9, -14及其组织抑制因子TIMP-1, -2, -3在恒河猴周期黄体发育不同阶段的协同表达. 结果显示: MMP-2 mRNA及其蛋白主要表达在早中期发育黄体的内皮细胞上, 在晚期黄体发生萎缩时则大量表达于黄体细胞; MMP-9, -14及其TIMP-1, -2, -3主要表达于黄体细胞; MMP-14 mRNA在早期和晚期黄体中高表达, MMP-9蛋白只在晚期黄体中高表达; TIMP-3蛋白在早、中、晚三期黄体中表达均较高, 但很明显晚期表达降低. 结果提示: MMP/TIMP系统参与灵长类黄体发育的调控, MMP-2, -14及其TIMP-1, -3可能参与黄体的形成和功能维持, 同时MMP-2, -9, -14及其TIMP-1, -2, -3在黄体萎缩期的协同表达, 提示它们可能在黄体发生萎缩时发挥作用. 相似文献
14.
15.
16.
17.
18.
19.
20.
Zhaoping He Qiusheng Tong Beate D. Quednau Kenneth D. Philipson Donald W. Hilgemann 《The Journal of general physiology》1998,111(6):857-873
We have cloned the squid neuronal Na+–Ca2+ exchanger, NCX-SQ1, expressed it in Xenopus oocytes, and characterized its regulatory and ion transport properties in giant excised membrane patches. The squid exchanger shows 58% identity with the canine Na+–Ca2+ exchanger (NCX1.1). Regions determined to be of functional importance in NCX1 are well conserved. Unique among exchanger sequences to date, NCX-SQ1 has a potential protein kinase C phosphorylation site (threonine 184) between transmembrane segments 3 and 4 and a tyrosine kinase site in the Ca2+ binding region (tyrosine 462). There is a deletion of 47 amino acids in the large intracellular loop of NCX-SQ1 in comparison with NCX1. Similar to NCX1, expression of NCX-SQ1 in Xenopus oocytes induced cytoplasmic Na+-dependent 45Ca2+ uptake; the uptake was inhibited by injection of Ca2+ chelators. In giant excised membrane patches, the NCX-SQ1 outward exchange current showed Na+-dependent inactivation, secondary activation by cytoplasmic Ca2+, and activation by chymotrypsin. The NCX-SQ1 exchange current was strongly stimulated by both ATP and the ATP-thioester, ATPγS, in the presence of F− (0.2 mM) and vanadate (50 μM), and both effects reversed on application of a phosphatidylinositol-4′,5′-bisphosphate antibody. NCX1 current was stimulated by ATP, but not by ATPγS. Like NCX1 current, NCX-SQ1 current was strongly stimulated by phosphatidylinositol-4′,5′-bisphosphate liposomes. In contrast to results in squid axon, NCX-SQ1 was not stimulated by phosphoarginine (5–10 mM). After chymotrypsin treatment, both the outward and inward NCX-SQ1 exchange currents were more strongly voltage dependent than NCX1 currents. Ion concentration jump experiments were performed to estimate the relative electrogenicity of Na+ and Ca2+ transport reactions. Outward current transients associated with Na+ extrusion were much smaller for NCX-SQ1 than NCX1, and inward current transients associated with Ca2+ extrusion were much larger. For NCX-SQ1, charge movements of Ca2+ transport could be defined in voltage jump experiments with a low cytoplasmic Ca2+ (2 μM) in the presence of high extracellular Ca2+ (4 mM). The rates of charge movements showed “U”-shaped dependence on voltage, and the slopes of both charge–voltage and rate–voltage relations (1,600 s−1 at 0 mV) indicated an apparent valency of −0.6 charges for the underlying reaction. Evidently, more negative charge moves into the membrane field in NCX-SQ1 than in NCX1 when ions are occluded into binding sites. 相似文献