Kvedar J, Levine L
J Invest Dermatol. 1987 Feb;88(2):124-9. doi: 10.1111/1523-1747.ep12525270.
Newborn rat keratinocytes, the NBR cell line, synthesized the cyclooxygenase metabolic products, prostaglandins E2 and F2 alpha, and the lipoxygenase metabolic product, hydroxyeicosatetraenoic acid. This metabolism was stimulated by incubation of the cells with the Ca++ ionophore, A23187; melittin; bradykinin; recombinant human f-met epidermal growth factor; the tumor promoter, 12-O-tetradecanoylphorbol-13-acetate; and the synthetic analog of diacylglycerol, 1-oleoyl-2-acetyl glycerol. Production of the cyclooxygenase products was inhibited by the synthetic glucocorticoid, dexamethasone. The stimulation appeared to be modulated by deesterification of arachidonic acid from the cellular lipids, presumably by phospholipase A2. Increased intracellular levels of Ca++ and phosphorylating activities that result from polyphosphoinositol turnover as well as phosphorylating activities independent of phosphatidylinositol turnover appear to be regulating phospholipase A2 hydrolysis of phospholipids.
新生大鼠角质形成细胞系NBR细胞能合成环氧化酶代谢产物前列腺素E2和F2α，以及脂氧合酶代谢产物羟基二十碳四烯酸。用钙离子载体A23187、蜂毒素、缓激肽、重组人f-甲硫氨酸表皮生长因子、肿瘤促进剂12-O-十四烷酰佛波醇-13-乙酸酯以及二酰基甘油的合成类似物1-油酰-2-乙酰甘油孵育细胞可刺激这种代谢。合成糖皮质激素地塞米松可抑制环氧化酶产物的生成。这种刺激似乎是由花生四烯酸从细胞脂质中的去酯化作用调节的，推测是通过磷脂酶A2。由多磷酸肌醇周转导致的细胞内钙离子水平升高和磷酸化活性，以及与磷脂酰肌醇周转无关的磷酸化活性，似乎在调节磷脂酶A2对磷脂的水解作用。
