PLC-gamma1 regulates fibronectin assembly and cell aggregation.
PLC-gamma1 regulates fibronectin assembly and cell aggregation.
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DOI：
10.1016/j.yexcr.2009.04.008
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发表时间：
2009-08-01
影响因子：
3.7
通讯作者：
Carpenter GF
中科院分区：
文献类型：
--
作者：
Crooke CE;Pozzi A;Carpenter GF
磷脂酶C-γ1（PLC-γ1）通过一种不确定的机制介导细胞粘附和迁移。在这里，我们研究PLC-γ1在细胞聚集的悬滴试验中在细胞-基质粘附中的作用。Plcg 1 β（−/−）小鼠胚胎成纤维细胞形成的聚集体比PLC-γ1重新表达的细胞（β +细胞）更大，对解离的抵抗力更强。聚集体的形成可以通过抑制纤连蛋白与整合素的相互作用来破坏，表明纤连蛋白组装可以介导聚集体的形成。在两种细胞系中，纤连蛋白组装均由整合素α5β1介导，而测量纤连蛋白组装的测定显示，在TGFAP细胞中组装增加。在脉冲标记实验中，E2和E3+细胞表现出相等的纤连蛋白mRNA水平和相等的纤连蛋白蛋白水平。然而，在条件培养基中分泌的纤连蛋白的水平增加，在p53细胞。这些数据暗示PLC-γ1通过控制纤连蛋白分泌到培养基中及其组装成原纤维而在细胞聚集中起负调节作用。
Phospholipase C-γ1 (PLC-γ1) mediates cell adhesion and migration through an undefined mechanism. Here, we examine the role of PLC-γ1 in cell-matrix adhesion in a hanging drop assay of cell aggregation. Plcg1 Null (−/−) mouse embryonic fibroblasts formed aggregates that were larger and significantly more resistant to dissociation than cells in which PLC-γ1 is re-expressed (Null + cells). Aggregate formation could be disrupted by inhibition of fibronectin interaction with integrins, indicating that fibronectin assembly may mediate aggregate formation. Fibronectin assembly was mediated by integrin α5β1 in both cell lines, while assays measuring fibronectin assembly revealed increased assembly in the Null cells. Null and Null + cells exhibited equivalent fibronectin mRNA levels and equivalent levels of fibronectin protein in pulse-labeling experiments. However, levels of secreted fibronectin in the conditioned medium were increased in Null cells. The data implicates a negative regulatory role for PLC-γ1 in cell aggregation by controlling the secretion of fibronectin into the media and its assembly into fibrils.
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影响因子：
2.7
作者：
LASH, JW;LINASK, KK;YAMADA, KM
通讯作者：
YAMADA, KM
影响因子：
4
作者：
Robinson, EE;Zazzali, KM;Foty, RA
通讯作者：
Foty, RA
影响因子：
8
作者：
Shepard, C. R.;Kassis, J.;Wells, A.
通讯作者：
Wells, A.
影响因子：
7.8
作者：
Nagai, T;Yamakawa, N;Aota, S;Yamada, S S;Akiyama, S K;Olden, K;Yamada, K M
通讯作者：
Yamada, K M
影响因子：
64.8
作者：
KUNDRA, V;ESCOBEDO, JA;ZETTER, BR
通讯作者：
ZETTER, BR