ADAM15 overexpression in NIH3T3 cells enhances cell-cell interactions
ADAM15 overexpression in NIH3T3 cells enhances cell-cell interactions
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DOI：
10.1006/excr.2001.5353
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发表时间：
2001-11-15
影响因子：
3.7
通讯作者：
Raines, EW
中科院分区：
文献类型：
--
作者：
Herren, B;Garton, KJ;Raines, EW
ADAM 15是金属蛋白酶-去整合素家族的成员，已显示其以RGD和非RGD依赖性方式与整合素相互作用。在本研究中，我们研究了ADAM 15过表达对NIH 3 T3细胞中细胞-基质和细胞-细胞相互作用的影响。四环素调节的ADAM 15在NIH 3 T3细胞中的过表达导致在Boyden室试验和划痕模型中纤连蛋白包被的过滤器上的迁移抑制。ADAM 15过表达对细胞迁移的影响不是由于基质附着的变化或缺乏对PDGF或纤连蛋白的细胞外信号调节激酶信号传导反应。然而，单层通透性的减少与ADAM 15过表达和改变细胞形态表明细胞间相互作用可能增加。NIH 3 T3细胞对逆转录病毒转导过表达ADAM 15的多克隆细胞群的粘附分析表明，与表达增强的绿色荧光蛋白的对照细胞相比，细胞粘附增加了45%。此外，我们证明了HA-表位标记的ADAM 15在上皮细胞系中形成广泛的细胞-细胞接触结构的细胞-细胞接触的定位。因此，过度表达。在NIH 3 T3细胞中的ADAM 15似乎增强了细胞-细胞相互作用，如通过减少细胞迁移、改变伤口边缘的细胞形态、降低单层渗透性以及通过逆转录病毒转导增加细胞与表达ADAM 15的细胞单层的粘附所表明的。(C)北京：科学出版社.
ADAM15 is a member of the family of metalloprotease-disintegrins that have been shown to interact with integrins in an RGD- and non-RGD-dependent manner. In the present study, we examined the effects of ADAM15 overexpression on cell-matrix and cell-cell interactions in NIH3T3 cells. Tetracycline-regulated ADAM15 overexpression in NIH3T3 cells leads to an inhibition of migration on a fibronectin-coated filter in a Boyden chamber assay and in a scratch wound model. The effects of ADAM15 overexpression on cell migration are not due to changes in matrix attachment or to the lack of extracellular signal-regulated kinase signaling response to PDGF or fibronectin. However, a decrease in monolayer permeability with ADAM15 overexpression and altered cell morphology suggest a possible increase in cell-cell interaction. Analysis of adhesion of NIH3T3 cells to a polyclonal population of cells retrovirally transduced to overexpress ADAM15 demonstrates a 45% increase in cell adhesion, compared with enhanced green fluorescent protein-expressing control cells. In addition, we demonstrate localization of HA-epitope-tagged ADAM15 to cell-cell contacts in an epithelial cell line that forms extensive cell-cell contact structures. Thus, overexpression. of ADAM15 in NIH3T3 cells appears to enhance cell-cell interactions, as suggested by decreased cell migration, altered cell morphology at the wound edge, decreased monolayer permeability, and increased cell adhesion to monolayers of cells expressing ADAM15 by retroviral transduction. (C) 2001 Academic Press.