Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad de Valencia, 46100-Burjassot, Valencia, Spain.
J Nutr Biochem. 2010 Mar;21(3):227-36. doi: 10.1016/j.jnutbio.2008.12.007. Epub 2009 Mar 9.
Vitamin A is essential for lung development and pulmonary cell differentiation and its deficiency results in alterations of lung structure and function. Basement membranes (BMs) are also involved in those processes, and retinoic acid, the main biologically active form of vitamin A, influences the expression of extracellular matrix macromolecules. Therefore, we have analyzed the ultrastructure and collagen content of lung alveolar BM in growing rats deficient in vitamin A and the recovering effect of all-trans retinoic acid. Male weanling pups were fed a retinol-adequate or -deficient diet until they were 60 days old. A group of vitamin A-deficient pups were recovered by daily intraperitoneal injections of all-trans retinoic acid for 10 days. Alveolar BM in vitamin A-deficient rats doubled its thickness and contained irregularly scattered collagen fibrils. Immunocytochemistry revealed that these fibrils were composed of collagen I. Total content of both collagen I protein and its mRNA was greater in vitamin-deficient lungs. In agreement with the greater size of the BM the amount of collagen IV was also increased. Proinflammatory cytokines, IL-1alpha, IL-1beta and TNF-alpha, did not change, but myeloperoxidase and TGF-beta1 were increased. Treatment of vitamin A-deficient rats with retinoic acid reversed all the alterations, but the BM thickness recovered only partially. Retinoic acid recovering activity occurred in the presence of increasing oxidative stress. In conclusion, vitamin A deficiency results in alterations of the structure and composition of the alveolar BM which are probably mediated by TGF-beta1 and reverted by retinoic acid. These alterations could contribute to the impairment of lung function and predispose to pulmonary disease.
维生素 A 对于肺的发育和肺细胞的分化是必需的,其缺乏会导致肺结构和功能的改变。基底膜 (BM) 也参与了这些过程,视黄酸是维生素 A 的主要生物活性形式,它影响细胞外基质大分子的表达。因此,我们分析了维生素 A 缺乏的生长大鼠肺肺泡 BM 的超微结构和胶原含量,以及全反式视黄酸的恢复效果。雄性断乳幼鼠用视黄醇充足或缺乏的饮食喂养,直到 60 天大。一组维生素 A 缺乏的幼鼠通过每天腹膜内注射全反式视黄酸 10 天来恢复。维生素 A 缺乏大鼠的肺泡 BM 厚度增加了一倍,并且含有不规则散布的胶原纤维。免疫细胞化学显示这些纤维由胶原 I 组成。维生素 A 缺乏肺中的胶原 I 蛋白及其 mRNA 的总量增加。与 BM 增大一致,胶原 IV 的量也增加了。促炎细胞因子 IL-1alpha、IL-1beta 和 TNF-alpha 没有改变,但髓过氧化物酶和 TGF-beta1 增加。用视黄酸治疗维生素 A 缺乏的大鼠逆转了所有的改变,但 BM 厚度仅部分恢复。视黄酸的恢复活性发生在氧化应激增加的情况下。总之,维生素 A 缺乏导致肺泡 BM 的结构和组成发生改变,这可能是由 TGF-beta1 介导的,并被视黄酸逆转。这些改变可能导致肺功能受损,并易患肺部疾病。