Schaefer H I, Höld K M, Egas-Kenniphaas J M, van der Laarse A
Department of Cardiology, University Hospital, Leiden, The Netherlands.
Cell Calcium. 1993 Jun;14(6):507-16. doi: 10.1016/0143-4160(93)90009-u.
The effect of lipoproteins on cellular calcium ion concentration ([Ca2+]i) in EA.hy 926 endothelial cells was investigated, particularly with respect to the difference in response on [Ca2+]i between native low-density lipoprotein (LDL) which binds to the apo B/E receptor, and acetylated LDL (AcLDL) which binds to the scavenger receptor. The scavenger receptor recognizes chemically or cell-induced modified LDL. LDL as well as AcLDL caused a transient increase of [Ca2+]i lasting 1-2 min. On a protein basis, LDL was more effective that AcLDL in raising [Ca2+]i. Preincubation of confluent cultures in growth medium with a reduced fetal bovine serum content (2% FBS instead of 10%) increased the potency of LDL to increase [Ca2+]i. The LDL-induced peak [Ca2+]i was dependent on cell density. The effect of AcLDL on [Ca2+]i did not differ between confluent and nonconfluent cultures. Also, preincubation with 2% FBS did not modify the AcLDL-induced calcium response. We conclude that binding of lipoproteins to membrane lipoprotein receptors is responsible for the transient rise of [Ca2+]i although the characteristics of the calcium response are dependent on the receptor involved, i.e. the apo B/E (LDL) receptor or the scavenger receptor. We suggest that Ca2+ acts as a second messenger, and that the LDL-induced calcium response is controlled by the proliferative state of the cells.
研究了脂蛋白对EA.hy 926内皮细胞中细胞钙离子浓度([Ca2+]i)的影响,特别是针对与载脂蛋白B/E受体结合的天然低密度脂蛋白(LDL)和与清道夫受体结合的乙酰化低密度脂蛋白(AcLDL)在[Ca2+]i反应上的差异。清道夫受体识别化学修饰或细胞诱导修饰的LDL。LDL以及AcLDL均引起[Ca2+]i的短暂升高,持续1 - 2分钟。以蛋白质计,LDL在升高[Ca2+]i方面比AcLDL更有效。将汇合培养物在胎牛血清含量降低(2% FBS而非10%)的生长培养基中预孵育,可增强LDL升高[Ca2+]i的能力。LDL诱导的[Ca2+]i峰值取决于细胞密度。AcLDL对[Ca2+]i的影响在汇合培养物和未汇合培养物之间没有差异。此外,用2% FBS预孵育不会改变AcLDL诱导的钙反应。我们得出结论,脂蛋白与膜脂蛋白受体的结合是[Ca2+]i短暂升高的原因,尽管钙反应的特征取决于所涉及的受体,即载脂蛋白B/E(LDL)受体或清道夫受体。我们认为Ca2+作为第二信使,并且LDL诱导的钙反应受细胞增殖状态的控制。