Povlsen Gro Klitgaard, Berezin Vladimir, Bock Elisabeth
ENKAM Pharmaceuticals, Copenhagen, Denmark.
J Neurochem. 2008 Feb;104(3):624-39. doi: 10.1111/j.1471-4159.2007.05033.x. Epub 2007 Nov 6.
The neural cell adhesion molecule (NCAM) plays important roles in neuronal development, regeneration, and synaptic plasticity. NCAM homophilic binding mediates cell adhesion and induces intracellular signals, in which the fibroblast growth factor receptor plays a prominent role. Recent studies on axon guidance in Drosophila suggest that NCAM also regulates the epidermal growth factor receptor (EGFR) (Molecular and Cellular Neuroscience, 28, 2005, 141). A possible interaction between NCAM and EGFR in mammalian cells has not been investigated. The present study demonstrates for the first time a functional interaction between NCAM and EGFR in mammalian cells and investigates the molecular mechanisms underlying this interaction. First, NCAM and EGFR are shown to play opposite roles in neurite outgrowth regulation in cerebellar granular neurons. The data presented indicate that negative regulation of EGFR is one of the mechanisms underlying the neuritogenic effect of NCAM. Second, it is demonstrated that expression of the NCAM-180 isoform induces EGFR down-regulation in transfected cells and promotes EGFR down-regulation induced by EGF stimulation. It is demonstrated that the mechanism underlying this NCAM-180-induced EGFR down-regulation involves increased EGFR ubiquitination and lysosomal EGFR degradation. Furthermore, NCAM-180-mediated EGFR down-regulation requires NCAM homophilic binding and interactions of the cytoplasmic domain of NCAM-180 with intracellular interaction partners, but does not require NCAM-mediated fibroblast growth factor receptor activation.
神经细胞黏附分子(NCAM)在神经元发育、再生及突触可塑性方面发挥着重要作用。NCAM的同源性结合介导细胞黏附并诱导细胞内信号,其中成纤维细胞生长因子受体起着重要作用。近期对果蝇轴突导向的研究表明,NCAM还可调节表皮生长因子受体(EGFR)(《分子与细胞神经科学》,28卷,2005年,第141页)。尚未对哺乳动物细胞中NCAM与EGFR之间可能存在的相互作用进行研究。本研究首次证实了哺乳动物细胞中NCAM与EGFR之间存在功能相互作用,并对这种相互作用的分子机制进行了研究。首先,在小脑颗粒神经元的神经突生长调节中,NCAM和EGFR发挥着相反的作用。所呈现的数据表明,EGFR的负调控是NCAM神经突生成效应的潜在机制之一。其次,研究表明,NCAM - 180异构体的表达可诱导转染细胞中EGFR下调,并促进EGF刺激诱导的EGFR下调。研究表明,这种由NCAM - 180诱导的EGFR下调的机制涉及EGFR泛素化增加和溶酶体对EGFR的降解。此外,NCAM - 180介导的EGFR下调需要NCAM同源性结合以及NCAM - 180胞质结构域与细胞内相互作用伙伴的相互作用,但不需要NCAM介导的成纤维细胞生长因子受体激活。