Expression of the ryanodine receptor isoforms in immune cells
Expression of the ryanodine receptor isoforms in immune cells
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DOI：
10.4049/jimmunol.167.9.4887
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发表时间：
2001-11-01
影响因子：
4.4
通讯作者：
Sei, Y
中科院分区：
文献类型：
--
作者：
Hosoi, E;Nishizaki, C;Sei, Y
Ryanodine受体（Ryanodine receptor，RYR）是介导细胞内钙释放的钙通道。我们已经使用RT-PCR分析，并检查其在原代外周血单个核细胞（PBMC）和164造血细胞系的表达。在PBMCs中，1型RYR（RYR 1）在CD 19（+）B淋巴细胞中表达，但在CD 3（+）T淋巴细胞和CD 14（+）单核细胞中表达较少。2型RYR（RYR 2）主要在CD 3 + T细胞中检测到。在用基质细胞衍生因子1、巨噬细胞炎性蛋白-1 α（MIP 1 α）或TGF-β处理后发现RYR 1和/或RYR 2 mRNA的诱导。在PBMC中未检测到3型RYR（RYR 3）。许多造血细胞系不仅表达RYR 1或RYR 2，而且还表达RYR 3。各亚型的表达与细胞系的特异性无关。我们发现，RYR刺激剂4-氯-间甲酚（4CmC）诱导Ca 2+释放，从而证实了RYR在表达RYR mRNA的细胞系中的功能表达。此外，在Jurkat T细胞中发现RYR mRNA与Ca 2+通道功能的一致诱导。在未处理的Jurkat T细胞中，4CmC（>1 mM）对Ca 2+释放没有影响，而4CmC（< 400 μ M）在用基质细胞衍生因子1、巨噬细胞炎性蛋白-1 α或TGF-β处理后诱导RYR 2和RYR 3后引起Ca 2+释放。我们的研究结果表明，所有三种异构体的RYR mRNA在造血细胞中的表达。响应于趋化因子和TGF-β的RYR的诱导表明在免疫应答期间在调节Ca 2+介导的细胞应答中的作用。
Ryanodine receptor (RYR) is a Ca2+ channel that mediates Ca2+ release from intracellular stores. We have used RT-PCR analysis and examined its expression in primary peripheral mononuclear cells (PBMCs) and in 164 hemopoietic cell lines. In PBMCs, type 1 RYR (RYR1) was expressed in CD19(+) B lymphocytes, but less frequently in CD3(+) T lymphocytes and in CD14(+) monocytes. Type 2 RYR (RYR2) was mainly detected in CD3(+) T cells. Induction of RYR1 and/or RYR2 mRNA was found after treatment with stromal cell-derived factor 1, macrophage-inflammatory protein-1 alpha (MIP1 alpha) or TGF-beta. Type 3 RYR (RYR3) was not detected in PBMCs. Many hemopoietic cell lines expressed not only RYR1 or RYR2 but also RYR3. The expression of the isoforms was not associated with specific cell lineage. We showed that the RYR-stimulating agent 4-chloro-m-cresol (4CmC) induced Ca2+ release and thereby confirmed functional expression of the RYR in the cell lines expressing RYR mRNA. Moreover, concordant induction of RYR mRNA with Ca2+ channel function was found in Jurkat T cells. In untreated Jurkat T cells, 4CmC (>1 mM) had no effect on Ca2+ release, whereas 4CmC (< 400 muM) caused Ca2+ release after the induction of RYR2 and RYR3 that occurred after treatment with stromal cell-derived factor 1, macrophage-inflammatory protein-1 alpha, or TGF-beta. Our results demonstrate expression of all three isoforms of RYR mRNA in hemopoietic cells. Induction of RYRs in response to chemokines and TGF-beta suggests roles in regulating Ca2+-mediated cellular responses during the immune response.