Llopis J, Kass G E, Duddy S K, Farell G C, Gahm A, Orrenius S
Department of Toxicology, Karolinska Institutet, Stockholm, Sweden.
FEBS Lett. 1991 Mar 11;280(1):84-6. doi: 10.1016/0014-5793(91)80209-l.
Hepatocyte tight junctional permeability has been shown to be regulated by hormones that exert their effects via phospholipase C activation. However, the precise transduction pathway involved in this effect is not known. The present study has employed the selective inhibitor of microsomal Ca2+ sequestration, 2,5-di(tert-butyl)-1,4-benzohydroquinone (tBuBHQ), to examine the effect of the mobilization of the endoplasmic reticular Ca2+ pool on tight junctional permeability in the perfused rat liver. Infusion of tBuBHQ followed by a bolus infusion of horseradish peroxidase (HRP) resulted in a significant increase in the first peak of biliary HRP, a measure of junctional permeability, whereas transcellular (vesicular) transport of HRP was not affected. Therefore, we conclude that the effect of hormones on tight junctional permeability is mediated, at least in part, by the mobilization of intracellular Ca2+.
肝细胞紧密连接通透性已被证明受通过激活磷脂酶C发挥作用的激素调节。然而,参与这种效应的确切转导途径尚不清楚。本研究采用微粒体Ca2+螯合的选择性抑制剂2,5-二(叔丁基)-1,4-苯二酚(tBuBHQ),来研究内质网Ca2+池的动员对灌注大鼠肝脏紧密连接通透性的影响。输注tBuBHQ后再推注辣根过氧化物酶(HRP),导致胆汁中HRP的第一个峰值显著增加,这是连接通透性的一个指标,而HRP的跨细胞(囊泡)转运不受影响。因此,我们得出结论,激素对紧密连接通透性的影响至少部分是由细胞内Ca2+的动员介导的。