Baeza-Squiban A, Boisvieux-Ulrich E, Delcher L, Marano F
Laboratoire de Cytophysiologie et Toxicologie cellulaire, Université Paris 7, France.
Toxicol Lett. 1998 Aug;96-97:245-51. doi: 10.1016/s0378-4274(98)00079-4.
A model of rabbit tracheal epithelial (RTE) cells in vitro was developed in order to investigate the effects, on the airway epithelium, of reactive oxygen species (ROS) generated by H2O2 in association or not in association with Fe2+. The immediate consequence of a 24 h exposure of RTE cells to an oxidative stress was an increase in catalase activity whereas superoxide dismutase activity was not modified. A latter consequence of a chronic ROS insult was the induction of a repair mechanism which led to squamous metaplasia (SM). SM is characterized by a stratification of the epithelium, the expression of the cytokeratin 13 and the appearance of cells with cross-linked envelopes. Reversible modifications between mucociliary and squamous phenotype are modulated by retinoids. The action of retinoids is selective: metaplasia is inhibited by agonists of RAR alpha and beta receptors and not by an agonist of RAR gamma receptors.
为了研究过氧化氢（H₂O₂）单独或与Fe²⁺联合产生的活性氧（ROS）对气道上皮的影响，建立了兔气管上皮（RTE）细胞的体外模型。RTE细胞暴露于氧化应激24小时的直接后果是过氧化氢酶活性增加，而超氧化物歧化酶活性未改变。慢性ROS损伤的后期后果是诱导了一种导致鳞状化生（SM）的修复机制。SM的特征是上皮分层、细胞角蛋白13的表达以及出现具有交联包膜的细胞。类视黄醇可调节黏液纤毛和鳞状表型之间的可逆性改变。类视黄醇的作用具有选择性：RARα和β受体激动剂可抑制化生，而RARγ受体激动剂则不能。
