E-cadherin interactions regulate β-cell proliferation in islet-like structures
E-cadherin interactions regulate β-cell proliferation in islet-like structures
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DOI：
10.1159/000107545
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发表时间：
2007-01-01
影响因子：
--
通讯作者：
Jones, Peter M.
中科院分区：
文献类型：
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作者：
Carvell, Melanie J.;Marsh, Phil J.;Jones, Peter M.
胰岛功能依赖于胰岛内的细胞相互作用。E-钙粘蛋白（ECAD）介导胰岛内B-细胞之间的Ca 2+依赖性嗜同性细胞粘附，并且已被鉴定为肿瘤抑制剂。我们产生了稳定过表达（S）和低表达（α S）ECAD的MIN 6 β细胞系的克隆。通过定量RT-PCR、免疫印迹和免疫细胞化学证实ECAD的修饰表达。前胰岛素原mRNA、胰岛素含量和胰岛素分泌的基础速率在S细胞中高于aS和对照（V）细胞。然而，刺激的胰岛素分泌反应不受ECAD表达水平的影响。ECAD表达确实影响增殖，ECAD表达增强与增殖降低相关，反之亦然。胰岛样结构的形成与V和S细胞增殖的显著减少有关，但与aS细胞无关。这些数据表明ECAD表达水平不调节胰岛素分泌功能，但与ECAD在β细胞增殖调节中的作用一致。
Islet function is dependent on cells within the islet interacting with each other. E- cadherin ( ECAD) mediates Ca2+- dependent homophilic cell adhesion between b- cells within islets and has been identified as a tumour suppressor. We generated clones of the MIN6 beta- cell line that stably over- ( S) and under-express ( alpha S) ECAD. Modified expression of ECAD was confirmed by quantitative RT- PCR, immunoblotting and immunocytochemistry. Preproinsulin mRNA, insulin content and basal rates of insulin secretion were higher in S cells compared to aS and control ( V) cells. However, stimulated insulin secretory responses were unaffected by ECAD expression levels. ECAD expression did affect proliferation, with enhanced ECAD expression being associated with reduced proliferation and vice versa. Formation of islet- like structures was associated with a significant reduction in proliferation of V and S cells but not aS cells. These data suggest that ECAD expression levels do not modulate insulin secretory function but are consistent with a role for ECAD in the regulation of beta-cell proliferation.