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鼠源分泌IgA的浆细胞瘤MOPC-315表达生长抑素受体。

The murine IgA-secreting plasmacytoma MOPC-315 expresses somatostatin receptors.

作者信息

Scicchitano R, Dazin P, Bienenstock J, Payan D G, Stanisz A M

机构信息

Department of Pathology, McMaster University, Hamilton, Ontario, Canada.

出版信息

J Immunol. 1988 Aug 1;141(3):937-41.

PMID:2899598
Abstract

We have previously shown that some neuropeptides had a profound effect on in vitro Ig synthesis (especially IgA) and mitogen-driven murine lymphocyte proliferation. MOPC-315, an IgA-secreting plasmacytoma line, has been extensively used in studies of the regulation of IgA synthesis. In this report we show that the neuropeptide somatostatin (SOM) inhibits proliferation ([3H]thymidine uptake) of MOPC-315 and also inhibits IgA synthesis in vitro. MOPC-315 cells bind both fluorescent SOM and [125I]SOM specifically. On cytofluorimetric analysis, 68 +/- 6.8% (mean +/- SE, n = 7) of MOPC 315 cells labeled with fluorescent SOM and this staining was compatible by incubation with an excess of unlabeled peptide. Specific [125I]SOM binding increased linearly with cell concentration, was rapid and achieved equilibrium after 20 min at 4 degrees C. It was temperature-dependent, readily reversible, and under equilibrium conditions demonstrated a dissociation constant of 1.6 +/- 0.7 nM (mean +/- SE, n = 5). Scatchard analysis showed that MOPC-315 cells had 40,733 +/- 16,050 (mean +/- SE) binding sites for SOM per cell. The characteristics of the interactions of SOM with MOPC-315 cells suggest a specific receptor-mediated mechanism whereby this neuropeptide may modulate lymphocyte function.

摘要

我们先前已表明,某些神经肽对体外Ig合成(尤其是IgA)以及丝裂原驱动的小鼠淋巴细胞增殖具有深远影响。MOPC - 315是一种分泌IgA的浆细胞瘤系,已广泛用于IgA合成调节的研究。在本报告中,我们表明神经肽生长抑素(SOM)可抑制MOPC - 315的增殖([3H]胸腺嘧啶核苷摄取),并且还可在体外抑制IgA合成。MOPC - 315细胞特异性结合荧光SOM和[125I]SOM。经细胞荧光分析,68±6.8%(平均值±标准误,n = 7)的MOPC 315细胞被荧光SOM标记,并且通过与过量未标记肽孵育,这种染色是相符的。特异性[125I]SOM结合随细胞浓度呈线性增加,速度很快,在4℃下20分钟后达到平衡。它是温度依赖性的,易于逆转,并且在平衡条件下显示解离常数为1.6±0.7 nM(平均值±标准误,n = 5)。Scatchard分析表明,MOPC - 315细胞每个细胞具有40,733±16,050(平均值±标准误)个SOM结合位点。SOM与MOPC - 315细胞相互作用的特征表明存在一种特异性受体介导的机制,通过该机制这种神经肽可能调节淋巴细胞功能。

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