Volume response of quiescent and interleukin 2-stimulated T-lymphocytes to hypotonicity.

Volume response of quiescent and interleukin 2-stimulated T-lymphocytes to hypotonicity.
复制标题

静止和白细胞介素 2 刺激的 T 淋巴细胞对低渗的体积反应。

DOI:
10.1152/ajpcell.1988.254.2.c286
复制
发表时间:
1988
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Deutsch,C
Deutsch,C
中科院分区:
--
文献类型:
--
作者:
Lee,SC;Price,M;Prystowsky,MB;Deutsch,C

文献摘要

被引文献

相似文献

淋巴细胞对低张力诱导的肿胀反应的调节体积减少(RVD)依赖于K+, Cl-和H2O的膜通透性。我们采用电子细胞定影、细胞水分测定和全细胞膜片钳法研究克隆小鼠t淋巴细胞L2的膜透性。静止的L2细胞表达低水平的电压门控K+通道,在25℃时不显示RVD。相反,用生长因子白介素2刺激增殖的L2细胞,在低张力下增加K+电导并显示RVD。受刺激细胞中的RVD被奎宁和维拉帕米阻断,其水平也完全阻断了电压门控的K+电导。肿胀的未受刺激的L2细胞可以通过添加一价阳离子离子包体gramicidin来诱导萎缩,而存在不适当的细胞外有机阳离子;革兰杀菌素还能提高受刺激细胞的RVD率。此外,阴离子运输抑制剂4,4'-二异硫氰基二苯乙烯-2,2'-二磺酸(DIDS)阻断了这种革兰杀菌素促进的RVD。这些结果表明,即使在未受刺激的L2细胞中也存在最小必要的Cl-通透性,必要的和限制性的K+通透性决定了RVD的速率,并且从电压门控K+电导的直接测量中可以预测,在生长因子刺激后,这种K+通透性增加。增殖的L2细胞的渗透性比静止的L2细胞约高70%。在37℃时,一些RVD发生在未受刺激的L2细胞中,受刺激的细胞表现出更快、更完全的收缩。这些结果讨论了潜在的膜通透性及其与受刺激细胞增殖的关系。
Regulatory volume decreased (RVD) in lymphocytes in response to hyptonically induced swelling is dependent on the membrane permeabilities of K+, Cl-, and H2O. We used electronic cell sizing, cell water determination, and the whole cell patch-clamp method to study these membrane permeabilities in the cloned mouse T-lymphocyte, L2. Quiescent L2 cells express low levels of a voltage-gated K+ channel and show no RVD at 25 degrees C. In contrast, L2 cells stimulated to proliferate with the growth factor interleukin 2 have increased K+ conductance and show RVD in response to hypotonicity. RVD in stimulated cells is blocked by quinine and verapamil at levels that also completely block the voltage-gated K+ conductance. Swollen, unstimulated L2 cells can be induced to shrink by addition of the monovalent cation ionophore gramicidin in the presence of impermeant extracellular organic cations; gramicidin also enhances the rate of RVD in stimulated cells. Additionally, the anion transport inhibitor 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) blocks this gramicidin-facilitated RVD. These results suggest that a minimum requisite Cl- permeability is present even in the unstimulated L2 cells, that a necessary and limiting K+ permeability determines the rate of RVD, and that this K+ permeability increases after growth-factor stimulation as predicted from the direct measurement of voltage-gated K+ conductance. The hydraulic permeability is approximately 70% greater in proliferating L2 cells than in quiescent cells. At 37 degrees C, some RVD occurs in unstimulated L2 cells, and stimulated cells show faster and more complete shrinkage. These results are discussed with respect to the underlying membrane permeabilities and their relation to stimulated cell proliferation.