P2X7受体作为成骨细胞中ERK激活的敏感流量传感器。
P2X7 receptor as sensitive flow sensor for ERK activation in osteoblasts.
作者信息
Okumura Hisashi, Shiba Dai, Kubo Toshikazu, Yokoyama Takahiko
机构信息
Department of Anatomy and Developmental Biology, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto 602-0841, Japan.
出版信息
Biochem Biophys Res Commun. 2008 Aug 1;372(3):486-90. doi: 10.1016/j.bbrc.2008.05.066. Epub 2008 May 22.
The involvement of the P2 receptor in the activation of ERK induced by a short transient fluid flow stimulation in MC3T3-E1 osteoblasts was examined in the current study. The ERK activation induced by this transient fluid flow stimulation was followed by an increase in c-fos mRNA expression. Suramin, a non-selective P2 receptor antagonist, and two different P2X7 receptor (P2X7R) antagonists, ATP analogue (oxidized ATP) and dye (Brilliant blue G), inhibited fluid flow-induced ERK activation. However, the P2Y receptor pathway inhibitor U73122 did not abolish this ERK activation. The P2X7R agonist 2',3'-O-(4-benzoylbenzoyl)-ATP (BzATP) significantly increased ERK activation and this activation could be completely inhibited by oxidized ATP and Brilliant blue G. Our results suggest that P2X7R is a highly sensitive P2 receptor for fluid flow-induced ERK activation in osteoblasts.
在本研究中，检测了P2受体在短暂瞬态流体流动刺激诱导的MC3T3-E1成骨细胞ERK激活中的作用。这种短暂瞬态流体流动刺激诱导的ERK激活之后是c-fos mRNA表达增加。苏拉明，一种非选择性P2受体拮抗剂，以及两种不同的P2X7受体（P2X7R）拮抗剂，ATP类似物（氧化ATP）和染料（亮蓝G），抑制了流体流动诱导的ERK激活。然而，P2Y受体途径抑制剂U73122并未消除这种ERK激活。P2X7R激动剂2'，3'-O-（4-苯甲酰苯甲酰基）-ATP（BzATP）显著增加ERK激活，并且这种激活可被氧化ATP和亮蓝G完全抑制。我们的结果表明，P2X7R是成骨细胞中流体流动诱导的ERK激活的高度敏感的P2受体。
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