Systemic Analysis of Tumor Cell-Induced Endothelial Calcium Signaling and Junction Disassembly.
Systemic Analysis of Tumor Cell-Induced Endothelial Calcium Signaling and Junction Disassembly.
复制标题
DOI：
10.1007/s12195-009-0067-5
复制
发表时间：
2009-09-01
影响因子：
2.8
通讯作者：
Dong, Cheng
中科院分区：
文献类型：
--
作者：
Peng, Hsin-Hsin;Dong, Cheng
在我们以前的研究中已经表明，黑色素瘤细胞以与磷脂酶C-钙激活相关的方式诱导连接解体。鉴于这一观察结果，我们已经开发了一个信号通路的数学模型，并采用多参数敏感性分析（MPSA）来确定模型中的重要参数，该模型研究了肿瘤细胞诱导的内皮细胞中的钙动员。生成钙动员模型的目标函数（相对于单个参数），并根据该函数进行MPSA。结果表明，肌浆网/内质网钙ATP酶可能是调节钙动员的关键因子之一。该模型是对信号网络进行系统分析的概念证明，其结果可能在描述内皮细胞如何响应肿瘤细胞方面具有实际应用。总而言之，我们设计了数值方法来宏观研究钙信号在与转移性肿瘤细胞接触的内皮细胞中的作用。
It has been shown in our previous study that melanoma cells induce junction disassembly in the manner related to phospholipase C-calcium activation. In light of this observation, we have developed a mathematical model of the signaling pathway and adapted multi-parametric sensitivity analysis (MPSA) to identify important parameters in the model, which examines tumor cell-induced calcium mobilization in endothelial cells. The objective functions, with respect to individual parameters, were generated for the calcium mobilization model and MPSA was performed according to the function. The results showed that sarco/endoplasmic reticulum calcium ATPase was one of the putative key factors in regulating calcium mobilization. The model is a proof of concept of systemic analysis of a signaling network, and the results may have practical applications in describing how endothelial cells respond to tumor cells. Taken together, we have devised numerical means to macroscopically study roles of calcium signaling in endothelial cells in contact with metastatic tumor cells.
登录
查看更多内容
影响因子：
3.1
作者：
Nwariaku, FE;Chang, JP;Turnage, RH
通讯作者：
Turnage, RH
DOI：
10.1177/0037549703040943
发表时间：
2003-12-01
影响因子：
1.6
作者：
Cho, KH;Shin, SY;Wolkenhauer, O
通讯作者：
Wolkenhauer, O
影响因子：
5.5
作者：
Sandoval, R;Malik, AB;Tiruppathi, C
通讯作者：
Tiruppathi, C
影响因子：
5.8
作者：
Sivakumaran, S;Hariharaputran, S;Bhalla, US
通讯作者：
Bhalla, US
影响因子：
3.1
作者：
Peng, HH;Hodgson, L;Dong, C
通讯作者：
Dong, C