Institute of Anatomy and Cell Biology, Justus-Liebig-University Giessen, Giessen, Germany.
Anat Rec (Hoboken). 2012 Feb;295(2):196-200. doi: 10.1002/ar.21543. Epub 2011 Dec 29.
Caveolin-1 (Cav-1) is highly expressed in alveolar epithelial type I (AE1) and endothelial cells of the alveolar region of the lung. Interestingly, alveolar epithelial type II (AE2) cells that are progenitors of the AE1 cells do not express Cav-1. We investigated whether genetic Cav-1 deficiency alters the phenotype of AE2 cells and their microenvironment using stereology. Total number, mean volume, and subcellular composition of the AE2 cells were not altered in Cav-1(-/-) when compared with wild-type mice. The alveolar septa were thickened and contained a significantly greater volume of extracellular matrix. Thus, AE2 cells as progenitors of AE1 cells are not critically involved in the severe pulmonary phenotype in Cav-1-deficient mice.
小窝蛋白-1（Cav-1）在肺泡上皮 I 型（AE1）和肺肺泡区域的内皮细胞中高度表达。有趣的是，作为 AE1 细胞前体的肺泡上皮 II 型（AE2）细胞不表达 Cav-1。我们使用体视学研究了 Cav-1 基因缺失是否会改变 AE2 细胞及其微环境的表型。与野生型小鼠相比，Cav-1(-/-)小鼠的 AE2 细胞总数、平均体积和亚细胞组成没有改变。肺泡间隔增厚，细胞外基质体积明显增大。因此，作为 AE1 细胞前体的 AE2 细胞并不在 Cav-1 缺陷型小鼠的严重肺部表型中起关键作用。
