Krueger G R, Stolzenburg T, Muller C
Pathology Institute, University of Cologne, F.R.G.
In Vivo. 1987 Nov-Dec;1(6):343-6.
Normal and malignant cells show differences in cell membrane lipid fluidity (CMF) which influence the expression of membrane receptors and may interfere with cell function. Friend virus (FLV) and Moloney virus (MLV) infected hematopoietic and lymphoid cells were monitored for CMF (fluorescence polarization) and for transferrin (TFC) and thymic (Thy) receptors (FITC-labelled monoclonal antibodies). CMF was modulated with cholesterol hemisuccinate (CHS), phospholipids (PL) and DMSO. Erythropoietic stem cells exhibit an increased persistent CMF within minutes after FLV infection; transferrin receptors are expressed, yet no hemoglobin is synthesized. CHS rigidification reduces TFC expression with differentiation of cells and hemoglobin synthesis, yet transformed cell populations do not react uniformly. Thymic lymphocytes, instead, do not exhibit changes in Thy expression upon CHS treatment although cell membranes become rigidified. Separate experiments showed these cells not being "transformed" per se but blocked in differentiation because of viral destruction of thymic epithelial cells with loss of thymopoietin in vivo. Thus viral cell transformation is followed by non-rigid but persistent membrane fluidization interfering with only selective receptor expression.
正常细胞和恶性细胞在细胞膜脂质流动性（CMF）方面存在差异，这会影响膜受体的表达，并可能干扰细胞功能。对感染了Friend病毒（FLV）和莫洛尼病毒（MLV）的造血细胞和淋巴细胞进行了CMF（荧光偏振）以及转铁蛋白（TFC）和胸腺（Thy）受体（异硫氰酸荧光素标记的单克隆抗体）的监测。用半琥珀酸胆固醇（CHS）、磷脂（PL）和二甲基亚砜调节CMF。红细胞生成干细胞在感染FLV后几分钟内表现出持续增加的CMF；转铁蛋白受体表达，但不合成血红蛋白。CHS使细胞膜刚性化，随着细胞分化和血红蛋白合成，TFC表达降低，但转化细胞群体的反应并不一致。相反，胸腺淋巴细胞在CHS处理后Thy表达没有变化，尽管细胞膜变得刚性化。单独的实验表明，这些细胞本身并未“转化”，而是由于体内胸腺上皮细胞被病毒破坏且胸腺生成素丧失而在分化过程中受阻。因此，病毒细胞转化后会出现非刚性但持续的膜流化，仅干扰选择性受体表达。
