PULMONARY SURFACTANT AND ITS COMPONENTS INHIBIT SECRETION OF PHOSPHATIDYLCHOLINE FROM CULTURED RAT ALVEOLAR TYPE-II CELLS
PULMONARY SURFACTANT AND ITS COMPONENTS INHIBIT SECRETION OF PHOSPHATIDYLCHOLINE FROM CULTURED RAT ALVEOLAR TYPE-II CELLS
复制标题
DOI：
10.1073/pnas.84.4.1010
复制
发表时间：
1987-02-01
影响因子：
11.1
通讯作者：
NELLENBOGEN, J
中科院分区：
文献类型：
--
作者：
DOBBS, LG;WRIGHT, JR;NELLENBOGEN, J
肺表面活性物质由肺泡II型细胞合成和分泌。放射性磷脂酰胆碱已被用作表面活性剂分泌的标志物。我们报告的结果表明，表面活性剂抑制分泌的3 H-标记的磷脂酰胆碱培养的大鼠II型细胞。Mr 26，000 - 36，000（SP 26-36）的脂质成分和表面活性蛋白基团对分泌有不同程度的抑制作用。表面活性剂脂质不完全抑制释放;在100 μ g/ml的浓度下，脂质抑制40%的刺激分泌，SP 26-36以0.1 μ g/ml的EC 50抑制释放。在1.0 μ g/ml的浓度下，SP 26-36抑制基础分泌并将由特布他林、佛波醇12-肉豆蔻酸酯13-乙酸酯和离子载体A23187刺激的分泌降低至基础水平。通过在加入SP 26-36后洗涤II型细胞，通过将蛋白质加热至100 ℃，可以阻断SP 26 - 36的抑制作用。通过加入对Sp 26-36特异性的抗血清，或通过在0.2mM EGTA存在下孵育细胞。从犬和人来源分离的SP 26-36也抑制大鼠II型细胞的磷脂酰胆碱释放。I型胶原和血清载脂蛋白A-1均不抑制分泌。这些发现与表面活性剂分泌受反馈调节控制的假设是一致的。
Pulmonary surfactant is synthesized and secreted by alveolar type II cells. Radioactive phosphatidylcholine has been used as a marker for surfactant secretion. We report findings that suggest that surfactant inhibits secretion of 3H-labeled phosphatidylcholine by cultured rat type II cells. The lipid components and the surfactant protein group of Mr 26,000-36,000 (SP 26-36) inhibit secretion to different extents. Surfactant lipids do not completely inhibit release; in concentrations of 100 .mu.g/ml, lipids inhibit stimulated secretion by 40%, SP 26-36 inhibits release with an EC50 of 0.1 .mu.g/ml. At concentrations of 1.0 .mu.g/ml, SP 26-36 inhibits basal secretion and reduces to basal levels secretion stimulated by terbutaline, phorbol 12-myristate 13-acetate, and the ionophore A23187. The inhibitory effect of SP 26-36 can be blocked by washing type II cells after adding SP 26-36, by heating the proteins to 100.degree. C for 10 min, by adding antiserum specific to Sp 26-36, or by incubating cells in the presence of 0.2 mM EGTA. SP 26-36 isolated from canine and human sources also inhibits phosphatidylcholine release from rat type II cells. Neither type I collagen nor serum apolipoprotein A-1 inhibits secretion. These findings are compatible with the hypothesis that surfactant secretion is under feedback regulatory control.