γ-干扰素上调K562细胞中的转铁蛋白受体并降低膜微粘度。

Gamma-interferon upregulates transferrin receptors and decreases membrane microviscosity in K562 cells.

作者信息

Iwagaki H, Marutaka M, Yoshino T, Cao L, Sakuma I, Uomoto M, Takeuchi Y, Tanaka N

机构信息

First Department of Surgery, Okayama University Medical School, Japan.

出版信息

Res Commun Mol Pathol Pharmacol. 1996 May;92(2):191-200.

PMID:8774072

Abstract

We investigated the effect of gamma-interferon (gamma-IFN) on three cellular parameters: cell membrane fluidity and expression of two antigens that have been associated with cell proliferation, namely transferrin receptor (Tf-R: a cell surface protein) and Ki-67 antigen (Ki-67: a nuclear protein). We observed small, yet significant changes in the first two parameters, but not the third parameter. These were investigated in K562 cells, a human chronic myelocytic leukemia cell line. These results suggest that the microviscosity changes and the surface Tf-R density were closely associated, and that gamma-IFN was involved in increasing proliferative activity of the cells by decreasing membrane fluidity and upregulating Tf-R expression.

摘要

我们研究了γ-干扰素（γ-IFN）对三个细胞参数的影响：细胞膜流动性以及与细胞增殖相关的两种抗原的表达，即转铁蛋白受体（Tf-R：一种细胞表面蛋白）和Ki-67抗原（Ki-67：一种核蛋白）。我们观察到前两个参数有微小但显著的变化，而第三个参数没有变化。这些研究是在K562细胞（一种人类慢性髓性白血病细胞系）中进行的。这些结果表明，微粘度变化与表面Tf-R密度密切相关，并且γ-IFN通过降低膜流动性和上调Tf-R表达参与增加细胞的增殖活性。