Arreola Jorge, Melvin James E
Center for Oral Biology in the Aab Institute of Biomedical Sciences and the Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
J Physiol. 2003 Feb 15;547(Pt 1):197-208. doi: 10.1113/jphysiol.2002.028373. Epub 2002 Dec 20.
Salivary gland fluid secretion is driven by transepithelial Cl- movement involving an apical Cl- channel whose molecular identity remains unknown. Extracellular ATP (ATP(o)) has been shown to activate a Cl- conductance (I(ATPCl)) in secretory epithelia; to gain further insight into I(ATPCl) in mouse parotid acinar cells, we investigated the effects of ATP(o) using the whole-cell patch-clamp technique. ATP(o) and 2'- and 3'-O-(4-benzoylbenzoyl)adenosine 5'-triphosphate triethylammonium salt (Bz-ATP) produced concentration-dependent, time-independent Cl- currents with an EC50 of 160 and 15 microM, respectively. I(ATPCl) displayed a selectivity sequence of SCN- > I- = NO3- > Cl- > glutamate, similar to the Cl- channels activated by Ca2+, cAMP and cell swelling in acinar cells. In contrast, I(ATPCl) was insensitive to pharmacological agents that are known to inhibit these latter Cl- channels, was independent of Ca2+ and was not regulated by cell volume. Moreover, the I(ATPCl) magnitude from wild-type animals was comparable to that from mice with null mutations in the Cftr, Clcn3 and Clcn2 Cl- channel genes. Taken together, our results demonstrate that I(ATPCl) is distinct from the channels described previously in acinar cells. The activation of I(ATPCl) by Bz-ATP suggests that P2 nucleotide receptors are involved. However, inhibition of G-protein activation with GDP-beta-S failed to block I(ATPCl), and Cibacron Blue 3GA and 4,4'-diisothyocyanostilbene-2,2'-disulphonic disodium salt selectively inhibited the Na+ currents (presumably through P2X receptors) without altering I(ATPCl), suggesting that neither P2Y nor P2X receptors are likely to be involved in I(ATPCl) activation. We conclude that I(ATPCl) is not associated with Cl- channels previously characterized in mouse parotid acinar cells, nor is it dependent on P2 nucleotide receptor stimulation. I(ATPCl) expressed in acinar cells reflects the activation of a novel ATP-gated Cl- channel that may play an important physiological role in salivary gland fluid secretion.
唾液腺液体分泌是由跨上皮Cl-移动驱动的,这涉及到一种顶端Cl-通道,其分子身份仍然未知。细胞外ATP(ATP(o))已被证明能激活分泌上皮中的Cl-电导(I(ATPCl));为了更深入了解小鼠腮腺腺泡细胞中的I(ATPCl),我们使用全细胞膜片钳技术研究了ATP(o)的作用。ATP(o)和2'-和3'-O-(4-苯甲酰苯甲酰)腺苷5'-三磷酸三乙铵盐(Bz-ATP)产生浓度依赖性、时间无关的Cl-电流,其EC50分别为160和15 microM。I(ATPCl)表现出SCN- > I- = NO3- > Cl- > 谷氨酸的选择性序列,类似于腺泡细胞中由Ca2+、cAMP和细胞肿胀激活的Cl-通道。相比之下,I(ATPCl)对已知抑制后一种Cl-通道的药物不敏感,不依赖于Ca2+,也不受细胞体积调节。此外,野生型动物的I(ATPCl)幅度与Cftr、Clcn3和Clcn2 Cl-通道基因无功能突变的小鼠相当。综上所述,我们的结果表明I(ATPCl)与腺泡细胞中先前描述的通道不同。Bz-ATP对I(ATPCl)的激活表明P2核苷酸受体参与其中。然而,用GDP-β-S抑制G蛋白激活未能阻断I(ATPCl),并且Cibacron Blue 3GA和4,4'-二异硫氰基芪-2,2'-二磺酸钠选择性抑制Na+电流(可能通过P2X受体)而不改变I(ATPCl),这表明P2Y和P2X受体都不太可能参与I(ATPCl)的激活。我们得出结论,I(ATPCl)与小鼠腮腺腺泡细胞中先前表征的Cl-通道无关,也不依赖于P2核苷酸受体刺激。腺泡细胞中表达的I(ATPCl)反映了一种新型ATP门控Cl-通道的激活,该通道可能在唾液腺液体分泌中发挥重要的生理作用。