Atomic force microscopy studies of functional and dysfunctional pulmonary surfactant films, II: albumin-inhibited pulmonary surfactant films and the effect of SP-A.
Atomic force microscopy studies of functional and dysfunctional pulmonary surfactant films, II: albumin-inhibited pulmonary surfactant films and the effect of SP-A.
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功能性和功能障碍性肺表面活性剂膜的原子力显微镜研究，II：白蛋白抑制的肺表面活性剂膜和 SP-A 的作用。
作者：
Y. Zuo;S. Tadayyon;E. Keating;Lin Zhao;R. Veldhuizen;N. Petersen;M. Amrein;F. Possmayer
血清蛋白渗入肺泡间隙引起的肺表面活性物质(PS)功能障碍可能是急性呼吸窘迫综合征的手术发病机制之一。白蛋白抑制PS是研究急性呼吸窘迫综合征表面活性物质异常的常用体外模型。然而，白蛋白抑制PS的机制仍然存在争议。用原子力显微镜研究了白蛋白抑制的牛脂提取物表面活性物质(BLES)在表面活性蛋白A(SP-A)作用下的膜结构。BLES和白蛋白(1：4W/W)从水介质共分散在空气-水界面上。共铺展使预吸附白蛋白分子对磷脂囊泡的吸附障碍最小，即由于竞争吸附而产生的抑制。原子力显微镜显示，与纯BLES单分子膜相比，薄膜结构有明显的变化，最高可达40mN/m。荧光共聚焦显微镜证实，当表面压力高于白蛋白的平衡表面压力时，白蛋白仍然留在单层的液体膨胀相中。剩余的白蛋白与BLES单层混合，以增加膜的可压缩性。这种抑制作用不能通过重复压缩-膨胀循环或添加表面活性蛋白A来解除。这些实验数据表明，血清蛋白对表面活性物质的抑制是一种新的机制，补充了传统的竞争吸附机制。
Pulmonary surfactant (PS) dysfunction because of the leakage of serum proteins into the alveolar space could be an operative pathogenesis in acute respiratory distress syndrome. Albumin-inhibited PS is a commonly used in vitro model for studying surfactant abnormality in acute respiratory distress syndrome. However, the mechanism by which PS is inhibited by albumin remains controversial. This study investigated the film organization of albumin-inhibited bovine lipid extract surfactant (BLES) with and without surfactant protein A (SP-A), using atomic force microscopy. The BLES and albumin (1:4 w/w) were cospread at an air-water interface from aqueous media. Cospreading minimized the adsorption barrier for phospholipid vesicles imposed by preadsorbed albumin molecules, i.e., inhibition because of competitive adsorption. Atomic force microscopy revealed distinct variations in film organization, persisting up to 40 mN/m, compared with pure BLES monolayers. Fluorescence confocal microscopy confirmed that albumin remained within the liquid-expanded phase of the monolayer at surface pressures higher than the equilibrium surface pressure of albumin. The remaining albumin mixed with the BLES monolayer so as to increase film compressibility. Such an inhibitory effect could not be relieved by repeated compression-expansion cycles or by adding surfactant protein A. These experimental data indicate a new mechanism of surfactant inhibition by serum proteins, complementing the traditional competitive adsorption mechanism.
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疏水性表面活性剂蛋白对肺表面活性剂单层塌陷的影响。
影响因子：
3.4
作者：
Lhert,Florence;Yan,Wenfei;Biswas,SamaresC;Hall,StephenB
通讯作者：
Hall,StephenB
血清对肺表面活性剂吸附的抑制以及亲水性聚合物逆转的机制：理论。
影响因子：
3.4
作者：
Zasadzinski,JosephA;Alig,TF;Alonso,Coralie;BernardinodelaSerna,Jorge;Perez-Gil,Jesus;Taeusch,HWilliam
通讯作者：
Taeusch,HWilliam
影响因子：
3.4
作者：
P. Stenger;J. Zasadzinski
通讯作者：
P. Stenger;J. Zasadzinski
肺表面活性剂磷脂的相行为与表面活性剂功能的经典模型之间的差异。
影响因子：
3.4
作者：
Piknova,B;Schief,WR;Vogel,V;Discher,BM;Hall,SB
通讯作者：
Hall,SB
DOI：
10.1164/ajrccm.155.4.9105072
发表时间：
1997-04-01
影响因子：
24.7
作者：
Gregory, TJ;Steinberg, KP;Gold, AJ
通讯作者：
Gold, AJ