Suwabe A, Takahashi K
Department of Laboratory Medicine, Yamagata University School of Medicine.
Nihon Kyobu Shikkan Gakkai Zasshi. 1993 Mar;31(3):317-23.
Surfactant protein A (SP-A) is known to inhibit surfactant secretion from pulmonary alveolar type II epithelial cells (type II cells). It is unknown whether SP-A acts as an inhibitor in the presence of lipids since SP-A mostly exists complexed with surfactant lipids. In this paper we focused on this issue using purified surfactant, purified SP-A and synthesized lipid liposomes. Surfactant secretion from type II cells was evaluated as TPA-stimulated secretion of radiolabeled lipids. The results demonstrated that 1) the inhibition of lipiD secretion by purified surfactant depended on its lipid components, not on the SP-A component, 2) the inhibitory effect of SP-A purified from surfactant was reversed in the presence of lipid liposomes, and 3) SP-A free from surfactant was unable to inhibit lipid secretion. We conclude from these results that SP-A can potentially inhibit surfactant secretion, but surfactant secretion is mainly regulated by surfactant lipids.
表面活性蛋白A(SP-A)已知可抑制肺泡II型上皮细胞(II型细胞)分泌表面活性剂。由于SP-A大多与表面活性剂脂质结合存在,所以在有脂质存在的情况下SP-A是否作为一种抑制剂尚不清楚。在本文中,我们使用纯化的表面活性剂、纯化的SP-A和合成脂质脂质体来关注这个问题。II型细胞的表面活性剂分泌通过佛波酯(TPA)刺激的放射性标记脂质分泌来评估。结果表明:1)纯化的表面活性剂对脂质分泌的抑制作用取决于其脂质成分,而非SP-A成分;2)从表面活性剂中纯化出的SP-A在脂质脂质体存在时抑制作用被逆转;3)不含表面活性剂的SP-A无法抑制脂质分泌。从这些结果我们得出结论,SP-A可能会抑制表面活性剂分泌,但表面活性剂分泌主要受表面活性剂脂质调节。