TERMINAL COMPLEMENT COMPLEX C5B-9 STIMULATES MITOGENESIS IN 3T3 CELLS
TERMINAL COMPLEMENT COMPLEX C5B-9 STIMULATES MITOGENESIS IN 3T3 CELLS
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DOI：
10.1172/jci116418
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发表时间：
1993-05-01
影响因子：
15.9
通讯作者：
NICHOLSONWELLER, A
中科院分区：
文献类型：
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作者：
HALPERIN, JA;TARATUSKA, A;NICHOLSONWELLER, A
补体的膜攻击复合物（MAC）可诱导细胞膜通透性的可逆变化，导致在不存在细胞溶解的情况下显著但短暂的细胞内离子变化。因为离子通量和胞质离子变化是当生长因子与其受体结合时启动的信号级联中不可或缺的步骤，我们假设MAC诱导的膜通透性的可逆变化可以刺激细胞增殖。使用纯化的末端补体成分，我们已经证明了MAC对静止小鼠3T3细胞的促有丝分裂作用。MAC增强了血清和PDGF的促有丝分裂作用，并且在没有其他外源性生长因子的情况下也刺激细胞增殖。MAC诱导的有丝分裂代表了末端补体复合物的一种新效应，其可能有助于补体激活部位局部的局灶性组织修复或病理性细胞增殖。
The membrane attack complex of complement (MAC) can induce reversible changes in cell membrane permeability resulting in significant but transient intracellular ionic changes in the absence of cell lysis. Because ion fluxes and cytosolic ionic changes are integral steps in the signaling cascade initiated when growth factors bind to their receptors, we hypothesized that the MAC-induced reversible changes in membrane permeability could stimulate cell proliferation. Using purified terminal complement components we have documented a mitogenic effect of the MAC for quiescent murine 3T3 cells. The MAC enhances the mitogenic effects of serum and PDGF, and also stimulates cell proliferation in the absence of other exogenous growth factors. MAC-induced mitogenesis represents a novel effect of the terminal complement complex that could contribute to focal tissue repair or pathological cell proliferation locally at sites of complement activation.