P2X purinergic receptor antagonist accelerates skin barrier repair and prevents epidermal hyperplasia induced by skin barrier disruption
P2X purinergic receptor antagonist accelerates skin barrier repair and prevents epidermal hyperplasia induced by skin barrier disruption
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DOI：
10.1046/j.1523-1747.2002.19505.x
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发表时间：
2002-11-01
影响因子：
6.5
通讯作者：
Denda, S
中科院分区：
文献类型：
--
作者：
Denda, M;Inoue, K;Denda, S
在无毛小鼠中评价ATP受体激动剂/拮抗剂对皮肤屏障恢复率的影响。局部应用ATP和α，β-亚甲基ATP（P2 X受体激动剂）延迟屏障恢复。在屏障破坏后局部应用苏拉明（非特异性ATP受体拮抗剂）、磷酸吡哆醛-6-偶氮苯基-2 '，4'-二磺酸（PPADS）（P2 X受体拮抗剂）和2 '，3'-O-（2，4，6-三硝基苯基）腺苷5 '-三磷酸（TNP-ATP）（P2 X1、P2 X3、P2 X2/3拮抗剂）加速屏障修复。P2 Y受体拮抗剂活性蓝2不影响屏障修复过程。此外，局部应用TNP-ATP防止低环境湿度下屏障损伤诱导的表皮增生。在器官培养中，在皮肤上胶带剥离后立即分泌ATP。α，β-亚甲基ATP使培养的角质形成细胞胞间钙离子浓度升高，这种升高可被TNP-ATP阻断。逆转录聚合酶链反应和免疫组织化学研究均表明，无毛小鼠表皮存在与P2 X3结构相似的蛋白。这些结果表明，皮肤屏障的稳态可以通过P2 X3样ATP受体的阳离子流量进行调节。
The effects of ATP receptor agonists/antagonists on skin barrier recovery rate were evaluated in hairless mice. Topical application of ATP and alpha,beta-methylene ATP (agonist of P2X receptor) delayed barrier recovery. Topical application of suramin (nonspecific ATP receptor antagonist), pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS) (P2X receptor antagonist), and 2',3'-O-(2,4,6-trinitrophenyl)adenosine 5'-triphosphate (TNP-ATP) (P2X1, P2X3, P2X2/3 antagonist) after barrier disruption accelerated the barrier repair. The P2Y type receptor antagonist Reactive Blue 2 did not affect the barrier repair process. Moreover, topical application of TNP-ATP prevented epidermal hyperplasia induced by barrier insult under low environmental humidity. ATP was secreted immediately after tape stripping on skin in organ culture. alpha,beta-Methylene ATP increased intercellular calcium in cultured keratinocytes and the increase was blocked by TNP-ATP. Both reverse transcription polymerase chain reaction assay and immunohistochemical study showed the existence of protein that had a structure similar to P2X3 on hairless mouse epidermis. These results suggest that cutaneous barrier homeostasis can be regulated by cation flux through a P2X3-like ATP receptor.