RGS13 controls g protein-coupled receptor-evoked responses of human mast cells.
RGS13 controls g protein-coupled receptor-evoked responses of human mast cells.
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DOI：
10.4049/jimmunol.181.11.7882
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发表时间：
2008-12-01
期刊：
影响因子：
--
通讯作者：
Druey KM
中科院分区：
文献类型：
--
作者：
Bansal G;DiVietro JA;Kuehn HS;Rao S;Nocka KH;Gilfillan AM;Druey KM
IgE-mediated mast cell degranulation and release of vasoactive mediators induced by allergens elicits allergic responses. Although G-protein-coupled receptor (GPCR)-induced signals may amplify IgE-dependent degranulation, how GPCR signaling in mast cells is regulated remains incompletely defined. We investigated the role of Regulator of G protein signaling (RGS) proteins in the modulation of these pathways in human mast cells. Several RGS proteins were expressed in mast cells including RGS13, which we previously showed inhibited IgE-mediated mast cell degranulation and anaphylaxis in mice. To characterize how RGS13 affects GPCR-mediated functions of human mast cells, we analyzed human mast cell lines (HMC-1 or LAD2) depleted of RGS13 by specific siRNA or shRNA and HMC-1 cells overexpressing RGS13. Transient RGS13 knockdown in LAD2 cells led to increased degranulation to sphingosine-1-phosphate, but not to antigen/IgE or C3a. Relative to control cells, HMC-1 cells stably expressing an RGS13-specific shRNA had greater Ca2+ mobilization in response to several GPCR ligands such as adenosine, C5a, sphingosine-1-phosphate (S-1P), and CXCL12 than wild-type cells. Akt phosphorylation, chemotaxis and cytokine (interleukin 8, IL-8) secretion induced by CXCL12 were also greater in shRGS13-HMC-1 cells compared to control. RGS13 overexpression inhibited CXCL12-evoked Ca2+ mobilization, Akt phosphorylation and chemotaxis. These results suggest that RGS13 restricts certain GPCR-mediated biological responses of human mast cells.
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影响因子：
4.4
作者：
Ali, H;Ahamed, J;Patel, DD
通讯作者：
Patel, DD
DOI：
10.1073/pnas.0703175104
发表时间：
2007-09-04
影响因子：
11.1
作者：
Costa, Carlotta;Barberis, Laura;Hirsch, Emilio
通讯作者：
Hirsch, Emilio
影响因子：
30.5
作者：
Bansal, Geetanjali;Xie, Zhihui;Druey, Kirk M.
通讯作者：
Druey, Kirk M.
影响因子：
5.5
作者：
Brightling, CE;Kaur, D;Bradding, P
通讯作者：
Bradding, P
影响因子：
32.4
作者：
Han, SB;Moratz, C;Kehrl, JH
通讯作者：
Kehrl, JH