PECAM-1 promotes β-catenin accumulation and stimulates endothelial cell proliferation
PECAM-1 promotes β-catenin accumulation and stimulates endothelial cell proliferation
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DOI：
10.1016/s0006-291x(03)00313-9
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发表时间：
2003-03-28
影响因子：
3.1
通讯作者：
Madri, JA
中科院分区：
文献类型：
--
作者：
Biswas, P;Canosa, S;Madri, JA
血小板内皮细胞粘附分子-1 (PECAM-1) 结合酪氨酸磷酸化 P-连环蛋白并调节 β-连环蛋白定位 [J.免疫学。 158（7）（1997）3408； J.细胞科学。 112（第 18 部分）（1999）3005]。为了阐明这种相互作用的功能后果，我们研究了来自 PECAM-1 敲除动物的内皮细胞，并将它们与表达 PECAM-1 的内皮细胞进行比较 [Mol.生物。细胞11（9）（2000）3109]。我们注意到表达 PECAM-1 的内皮细胞中 P-catenin 蛋白的表达增加。此外，通过免疫荧光，β-连环蛋白定位于PECAM-1阳性内皮细胞的细胞膜和细胞核，而不表达PECAM-1的细胞仅在膜上对β-连环蛋白进行染色。此外，我们证明，与全长 PECAM-1 相比，缺乏大部分胞质结构域的 PECAM-1 会显着减少转录活性 β-连环蛋白的积累。最后，我们注意到与缺乏 PECAM-1 的内皮细胞相比，PECAM-1 重组细胞的增殖率增加。综上所述，我们的数据表明 PECAM-1（一种粘附分子）通过转录活性 β-连环蛋白的积累影响细胞增殖。 (C) 2003 年爱思唯尔科学（美国）。版权所有。
Platelet endothelial cell adhesion molecule-1 (PECAM-1) binds tyrosine phosphorylated P-catenin and modulates beta-catenin localization [J. Immunol. 158 (7) (1997) 3408; J. Cell Sci. 112 (Pt 18) (1999) 3005]. To elucidate functional consequences of this interaction, we studied endothelial cells from PECAM-1 knockout animals and compared them to PECAM-1 expressing endothelial cells [Mol. Biol. Cell 11 (9) (2000) 3109]. We noted an increase in the expression of P-catenin protein in PECAM-1 expressing endothelial cells. Further, by immunofluorescence, beta-catenin localized to the cell membrane as well as to the nucleus in PECAM-1 positive endothelial cells, whereas cells not expressing PECAM-1 stained for beta-catenin only at the membrane. Additionally, we demonstrate that PECAM-1 lacking the majority of the cytoplasmic domain promotes significantly less accumulation of transcriptionally active beta-catenin than full-length PECAM-1. Finally, we note an increased proliferative rate in the PECAM-1 reconstituted cells compared to the endothelial cells lacking PECAM-1. Taken together, our data suggest that PECAM-1, an adhesion molecule, affects cell proliferation via accumulation of transcriptionally active beta-catenin. (C) 2003 Elsevier Science (USA). All rights reserved.