Erythrocytes store and release sphingosine 1-phosphate in blood

Erythrocytes store and release sphingosine 1-phosphate in blood
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DOI:
10.1096/fj.06-7433com
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发表时间:
2007-04-01
期刊:
影响因子:
4.8
通讯作者:
Graeler, Markus H.
Graeler, Markus H.
中科院分区:
生物学2区
文献类型:
--
作者:
Haenel, Petra;Andreani, Paul;Graeler, Markus H.

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血液成分鞘氨醇1-磷酸(S1 P)是五种G蛋白偶联受体的特异性配体,命名为S1 P(1-5)。淋巴细胞上S1 P(1)受体的表达是淋巴细胞从次级淋巴器官中排出所必需的,这表明S1 P是维持血液中淋巴细胞循环的刺激物。尽管其在免疫监视中的潜在作用,但控制血液S1 P水平的调节系统尚不清楚。这份报告表明,红细胞构成了血液中S1 P的缓冲系统。它们有效地整合和储存S1 P,并保护其免受细胞降解。它们还将S1 P释放到血浆中,但不释放到其他无血清培养基中,表明S1 P释放受血浆因子控制。红细胞不产生S1 P,因为血浆S1 P水平的增加总是伴随着细胞S1 P水平的降低。据报道,活化后产生和释放S1 P的血小板对血液中观察到的S1 P释放没有贡献。培养基中红细胞的量以及血浆的比例决定了S1 P释放的幅度。连续转移S1 P负载和卸载小鼠红细胞显示正常的寿命和相似的S1 P水平恢复后24小时,表明S1 P的掺入和释放在体内动态调节。
The blood constituent sphingosine 1-phosphate (S1P) is a specific ligand for five G-protein-coupled receptors designated S1P(1-5). Expression of the S1P(1) receptor on lymphocytes is required for their exit from secondary lymphoid organs, suggesting that S1P serves as a stimulus for maintaining lymphocyte circulation in blood. Despite its potential role in immune surveillance, the regulatory system that controls blood S1P levels is not well understood. This report reveals that erythrocytes constitute a buffer system for S1P in blood. They efficiently incorporated and stored S1P, and protected it from cellular degradation. They also released S1P into plasma, but not into other serum-free media, indicating that S1P release was controlled by a plasma factor. Erythrocytes did not generate S1P since an increase in plasma S1P levels was always accompanied by a decrease in cellular S1P levels. Thrombocytes that were reported to generate and release S1P after activation did not contribute to the observed S1P release in blood. The amount of erythrocytes as well as the proportion of plasma in the medium determined the magnitude of S1P release. Adoptively transferred S1P-loaded and unloaded mouse erythrocytes displayed a normal life span and similar S1P levels 24 h after recovery, indicating that S1P incorporation and release are dynamically regulated in vivo.