Intracellular adenosine inhibits IgE-dependent degranulation of human skin mast cells.
Intracellular adenosine inhibits IgE-dependent degranulation of human skin mast cells.
复制标题
细胞内腺苷抑制人类皮肤肥大细胞的IgE依赖性脱粒。
DOI：
10.1007/s10875-013-9950-x
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发表时间：
2013-11
影响因子：
9.1
通讯作者：
Schwartz LB
中科院分区：
文献类型：
--
作者：
Gomez G;Nardone V;Lotfi-Emran S;Zhao W;Schwartz LB
Adenosine (ADO) can enhance and inhibit mast cell degranulation. Potentiation of degranulation occurs at relatively low concentrations of ADO (10−6–10−5 M) through triggering of A3AR, whereas, inhibition occurs at higher concentrations of ADO reportedly through triggering of A2aAR. However, the discrepancy in the concentration of ADO that inhibits degranulation and that required to trigger ADORs suggests a different mechanism. The purpose of this study is to determine the mechanism by which ADO inhibits human mast cell degranulation. We compare the effectiveness of A2aAR specific antagonist ZM241385 and equilibrative nucleoside transporter inhibitors Dipyridamole and NBMPR in preventing ADO-mediated inhibition of FcεRI-induced degranulation of human skin mast cells (hSMCs). Western blotting is done to analyze the effect of ADO on FcεRI-induced Syk phosphorylation. Dipyridamole and NBMPR completely and dose-dependently prevented ADO from inhibiting FcεRI-induced degranulation in all hSMC preparations. In contrast, ZM241385 at 10−5 M was effective in only 3 of 10 hSMC preparations. Moreover, NBMPR was effective even in those hSMC preparations not responsive to ZM241385. ADO inhibited degranulation induced by FcεRI crosslinking, but not that induced by complement component 5a (C5a), Substance P or calcium ionophore. Accordingly, ADO significantly attenuated FcεRI-induced phosphorylation of Syk at the critical activating tyrosine (Y525). Blocking the influx of ADO, but not A2aAR signals, is necessary and sufficient to prevent ADO from inhibiting FcεRI-induced mast cell degranulation. Thus, ADO specifically inhibits FcεRI-induced degranulation of hSMCs primarily by an intracellular mechanism that requires its influx via equilibrative nucleoside transporter 1 (ENT1).
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影响因子：
5.4
作者：
Duffy, S Mark;Cruse, Glenn;Brightling, Christopher E;Bradding, Peter
通讯作者：
Bradding, Peter
影响因子：
7.3
作者：
HILLYARD, PA;NIALS, AT;VARDEY, CJ
通讯作者：
VARDEY, CJ
影响因子：
5.8
作者：
HUGHES, PJ;HOLGATE, ST;CHURCH, MK
通讯作者：
CHURCH, MK
DOI：
10.1164/ajrccm/138.5.1143
发表时间：
1988-11-01
期刊：
AMERICAN REVIEW OF RESPIRATORY DISEASE
影响因子：
--
作者：
PEACHELL, PT;COLUMBO, M;MARONE, G
通讯作者：
MARONE, G
影响因子：
2.8
作者：
DRAKE, I;ROUTLEDGE, PA;RICHARDS, R
通讯作者：
RICHARDS, R