Correlation of Alterations in Cation Exchange and Sarcolemmal Ultrastructure Produced by Neuraminidase and Phospholipases in Cardiac Cell Tissue Culture

Correlation of Alterations in Cation Exchange and Sarcolemmal Ultrastructure Produced by Neuraminidase and Phospholipases in Cardiac Cell Tissue Culture
复制标题

心肌细胞组织培养中神经氨酸酶和磷脂酶产生的阳离子交换与肌膜超微结构变化的相关性

DOI:
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发表时间:
1981
影响因子:
20.1
通讯作者:
K. Philipson
K. Philipson
中科院分区:
医学1区
文献类型:
--
作者:
G. Langer;J. Frank;K. Philipson

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将来自新生儿腐烂心脏的培养物中的成肌细胞和成纤维细胞暴露于神经氨酸酶和磷脂酶 C (PLC) 和 Ai (PLAi)。在酶暴露之前和之后测量细胞的钙(Ca)和钾(K)交换。对照和处理细胞的交换特征与细胞超微结构相关,包括评估膜内颗粒(IMP)密度和通过冷冻断裂聚集。已知神经氨酸酶暴露(去除唾液酸)可显着增加成肌细胞的钙渗透性,而不改变钾渗透性,但不会导致这些细胞的 IMP 构型发生变化。然而,PLC 使 Ca 和 K 渗透性显着增加,允许 La 进入,并且与成肌细胞中的 IMP 聚集相关。 PLAi 不会改变成肌细胞的离子渗透性,也不会改变膜内颗粒的构型。成纤维细胞暴露于 PLC 后,Ca 或 K 渗透性没有变化,IMP 分布也没有变化。这些结果与先前对唾液酸去除引起的渗透性变化的研究相结合,表明细胞 Ca 渗透性的控制存在于细胞表面的至少两个独立位点:(1)糖萼和(2)脂质双层。相比之下,K 渗透性控制基于双层内。超微结构相关性表明 IMP 聚集可能与双层通透性的变化有关。
Myoblasts and fibroblasts in cultures derived from neonatal rot hearts were exposed to neuraminidase and phospholipases C (PLC) and Ai (PLAi). Calcium (Ca) and potassium (K) exchange of the cells waa measured before and after enzymatic exposure. The exchange characteristics of control and treated cells were correlated with cellular ultrastructure including assessment of intramembrane particle (IMP) density and aggregation by freeze-fracture. Neuraminidase exposure (removal of sialic acid) known to produce marked increase in calcium permeability without change in potassium permeability in myoblasts produced no change in IMP configuration of these cells. PLC, however, produced marked increase hi both Ca and K permeabilities, permitted entry of La, and was associated with IMP aggregation in myoblastic cells. PLAi produced no change in ionic permeability and no alteration in intramembrane particle configuration in myoblasts. Exposure of fibroblasts to PLC caused no change in either Ca or K permeability and no change in IMP distribution. These results, coupled with those of previous studies of permeability changes induced by sialic acid removal, indicate that control of cellular Ca permeability resides in at least two separate sites at the cellular surface: (1) the glycocalyx and (2) the lipid bilayer. By contrast, K permeability control is based within the bilayer. Ultrastructural correlations suggest that IMP aggregation may be associated with changes in bilayer permeability.