Chalfant M L, Civan J M, Peterson-Yantorno K, DiBona D R, O'Brien T G, Civan M M
Department of Physiology, University of Pennsylvania, Philadelphia, PA 19104-6085, USA.
J Membr Biol. 1996 Aug;152(3):207-15. doi: 10.1007/s002329900098.
Protein kinase C (PKC) is a major regulator of a broad range of cellular functions. Activation of PKC has been reported to stimulate Na+ transport across frog skin epithelium by increasing the apical Na+ permeability. This positive natriferic response has not been observed with other epithelial preparations, and could reflect the specific experimental conditions of different laboratories, or species or organ specificity of the response to PKC. In the present study, measurements were conducted with skins and urinary bladders from the same animals of two different species. The PKC activator TPA uniformly increased the transepithelial Na+ transport (measured as amiloride-sensitive short-circuit current, ISC, across skins from Rana temporaria and Bufo marinus, and inhibited ISC across bladders from the same animals. Inhibitors of PKC (staurosporine, H-7 and chelerythrine) partially blocked the TPA-induced stimulation of ISC across frog skin. The specificity of the PKC response by amphibian skin could have reflected an induction of moulting, similar to that observed with aldosterone. However, light micrographs of paired areas of frog skin revealed no evidence of the putative moulting. Separation of stratum corneum from the underlying stratum granulosum could be detected following application of aldosterone. We conclude that the effect of PKC on epithelial Na+ channels is organ, and not species specific. The stimulation of Na+ permeability in amphibian skin does not arise from sloughing of the stratum corneum. These observations are consistent with the hypothesis that the natriferic action arises from the calcium-independent isozyme of PKC previously detected in frog skin.
蛋白激酶C（PKC）是多种细胞功能的主要调节因子。据报道，PKC的激活可通过增加顶端Na⁺通透性来刺激蛙皮上皮细胞的Na⁺转运。在其他上皮组织中未观察到这种正向促钠反应，这可能反映了不同实验室的特定实验条件，或对PKC反应的物种或器官特异性。在本研究中，对来自两个不同物种的同一动物的皮肤和膀胱进行了测量。PKC激活剂佛波酯（TPA）一致地增加了跨上皮Na⁺转运（以氨氯地平敏感的短路电流，即ISC来衡量，该电流通过林蛙和海蟾蜍的皮肤，并抑制了来自同一动物膀胱的ISC。PKC抑制剂（星形孢菌素、H-7和白屈菜红碱）部分阻断了TPA诱导的蛙皮ISC刺激。两栖动物皮肤对PKC反应的特异性可能反映了蜕皮的诱导，类似于醛固酮所观察到的情况。然而，蛙皮配对区域的光学显微镜照片未显示假定蜕皮的证据。应用醛固酮后可检测到角质层与下层颗粒层的分离。我们得出结论，PKC对上皮Na⁺通道的作用是器官特异性的，而非物种特异性的。两栖动物皮肤中Na⁺通透性的刺激并非源于角质层的脱落。这些观察结果与以下假设一致，即促钠作用源于先前在蛙皮中检测到的PKC钙非依赖性同工酶。
