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Extracellular ATP induces CD44 shedding from macrophage-like P388D1 cells via the P2X7 receptor

机译:细胞外ATP通过P2X7受体诱导巨噬细胞样P388D1细胞CD44脱落

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摘要

The P2X7 receptor (P2X7R) is a nucleotide receptor expressed predominantly on hemopoietic, bone, and epithelial cells. The P2X7R can be activated by extracellular ATP and induces the influx of calcium, releases cytokines, and participates in cell proliferation and apoptosis. CD44 is an adhesion molecule. The effects of CD44 include cell-cell and cell-matrix adhesion interactions, lymphocyte activation, and cell migration. Many studies have shown that P2X7R and CD44 play important roles in hematological malignancies, but no study exists regarding the relationship between P2X7R and CD44. In the present study, we characterized P388D1 cells for the surface expression of CD44 and analyzed ATP-induced shedding. The data showed that P388D1 cells express CD44. Incubation of P388D1 cells with ATP induced a rapid loss of CD44 from the P388D1 cell surface. In addition, using a receptor inhibitor and P2X7R short hairpin RNA, we showed that the loss of CD44 is mediated via the P2X7R. Finally, we demonstrated that activation of P2X7R by ATP induces CD44 shedding.
机译:P2X7受体(P2X7R)是主要在造血,骨骼和上皮细胞上表达的核苷酸受体。 P2X7R可以被细胞外ATP激活,诱导钙的流入,释放细胞因子,并参与细胞增殖和凋亡。 CD44是粘附分子。 CD44的作用包括细胞-细胞和细胞-基质粘附相互作用,淋巴细胞活化和细胞迁移。许多研究表明,P2X7R和CD44在血液系统恶性肿瘤中起重要作用,但是关于P2X7R和CD44之间的关系尚无研究。在本研究中,我们表征了P388D1细胞CD44的表面表达并分析了ATP诱导的脱落。数据显示,P388D1细胞表达CD44。将P388D1细胞与ATP一起孵育会诱导CD44从P388D1细胞表面迅速丢失。此外,使用受体抑制剂和P2X7R短发夹RNA,我们显示CD44的丢失是通过P2X7R介导的。最后,我们证明了ATP激活P2X7R会诱导CD44脱落。

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