Arvidson G, Johansson P, Josefsson J O
Eur J Cell Biol. 1982 Aug;28(1):27-33.
Low temperature inhibited preferentially pinocytosis induced by Na+ and Na+-like inducers, a category of inducers which are particularly dependent on the concentration of Ca++ that means susceptible to blockade by EGTA, La+++, or high Ca++. Coldness inhibited Na+-induced pinocytosis more effectively in cells from a calcium deficient medium than in normal cells and the inhibition was abolished by Ca++. In normally fed cells, a period of coldness prevented the subsequent induction of pinocytosis by Na+. This block was of the same type as that observed when the concentration of Ca++ was increased in the medium of normal cells kept at room temperature. In contrast, starved cells responded to coldness by an increased capacity for pinocytosis. These effects lasted for several hours after the cells had been rewarmed and were mediated by a cell-derived soluble factor, PRF, pinocytosis regulating factor. Solubility characteristics indicated that PRF is a lipid. Ca++, low pH, and low temperature stimulated accumulation of the factor in the medium. Preincubation with PRF or addition of PRF to the inducer stimulated pinocytosis in starved or Ca++-deficient cells and reduced the sensitivity to Na+-like inducers in normal cells. The amount of PRF secreted from cold cells was sufficient to cause the Ca++-like blockade of pinocytosis in the cold, the diminished pinocytotic activity after a cold period and the activating effect of coldness on starved cells. PRF appears to be an important physiological regulator of the capacity for pinocytosis in the amoeba.
低温优先抑制由Na⁺及类Na⁺诱导剂所诱导的胞饮作用，这类诱导剂特别依赖Ca²⁺的浓度，这意味着它们易受乙二醇双四乙酸（EGTA）、镧离子（La³⁺）或高浓度Ca²⁺的阻断。低温对来自缺钙培养基的细胞中Na⁺诱导的胞饮作用的抑制比正常细胞更有效，且这种抑制作用可被Ca²⁺消除。在正常喂养的细胞中，一段时间的低温可阻止随后由Na⁺诱导的胞饮作用。这种阻断与在室温下保持的正常细胞培养基中Ca²⁺浓度增加时所观察到的阻断类型相同。相比之下，饥饿细胞对低温的反应是胞饮能力增强。这些效应在细胞复温后持续数小时，并由一种细胞衍生的可溶性因子——胞饮作用调节因子（PRF）介导。溶解性特征表明PRF是一种脂质。Ca²⁺、低pH值和低温会刺激该因子在培养基中的积累。用PRF预孵育或向诱导剂中添加PRF可刺激饥饿或缺钙细胞中的胞饮作用，并降低正常细胞对类Na⁺诱导剂的敏感性。低温细胞分泌的PRF量足以在低温下引起类似Ca²⁺对胞饮作用的阻断、低温处理后胞饮活性的降低以及低温对饥饿细胞的激活作用。PRF似乎是变形虫胞饮能力的一种重要生理调节因子。
