Tamm I, Kikuchi T, Kreutter D, Pledger W J, Pfeffer L M
Rockefeller University, New York, NY 10021.
J Interferon Res. 1994 Oct;14(5):265-73. doi: 10.1089/jir.1994.14.265.
Interferon-alpha/beta (IFN-alpha/beta) suppresses cell cycle activation by platelet-derived growth factor (PDGF) as well as the induction of the 31-kD (pI) and the 35-kD (pII) proteins in density-arrested BALB/c-3T3 cells. We report that elevation of [Ca2+]i by ionomycin induces the synthesis of the 31-kD protein, but not that of the 35-kD protein. Since IFN blocks the PDGF-induced elevation of [Ca2+]i, these results suggest that IFN treatment may suppress pI induction by impairing this PDGF-activated signal transduction pathway. In contrast, because ionomycin did not induce the 35-kD protein, the suppression by IFN of PDGF-induced pII appears to be mediated via a pathway distinct from that operating in the suppression of pI. In BALB/c-3T3 cells, IFN-alpha/beta did not itself affect the turnover or de novo synthesis of inositol phospholipids and the cellular content of diacylglycerol, nor did IFN block the enhancement of these parameters by PDGF.
α/β干扰素（IFN-α/β）可抑制血小板衍生生长因子（PDGF）激活的细胞周期，以及在密度抑制的BALB/c - 3T3细胞中诱导31-kD（pI）和35-kD（pII）蛋白的表达。我们报道，离子霉素升高细胞内钙离子浓度（[Ca2+]i）可诱导31-kD蛋白的合成，但不能诱导35-kD蛋白的合成。由于IFN可阻断PDGF诱导的[Ca2+]i升高，这些结果提示IFN处理可能通过损害这种PDGF激活的信号转导途径来抑制pI的诱导。相反，由于离子霉素不能诱导35-kD蛋白，IFN对PDGF诱导的pII的抑制作用似乎是通过一条不同于抑制pI的途径介导的。在BALB/c - 3T3细胞中，IFN-α/β本身并不影响肌醇磷脂的周转或从头合成以及二酰甘油的细胞含量，IFN也不阻断PDGF对这些参数的增强作用。
