Meeting Abstract
P1.158 Saturday, Jan. 4 15:30 Effects of thyroid hormones and glucocorticoids on lung development in metamorphosing Xenopus laevis tadpoles YAO, A*; CLARK, F; TEMKIN, M; SCHREIBER, A.M.; St. Lawrence University, NY; Bard College, NY; St. Lawrence University, NY; St. Lawrence University, NY aschreiber@stlawu.edu
Prior to metamorphosis, the primary respiratory surfaces of X. laevis tadpoles are the skin and gills. Although tadpoles do have functional lungs as early as hatching, their contribution to respiration at this developmental stage is thought to be minor. However, following the abrupt loss of the gills and thickening of the skin during metamorphosis, the lungs rapidly take on a more prominent respiratory role. Thyroid hormone (TH) and glucocorticoids (GC) are known to play important roles in mammalian post-natal lung development, and have also been shown to work synergistically to mediate most, if not all, aspects of amphibian metamorphosis. In order to determine the influence of these hormones on metamorphic lung development, pro-metamorphic tadpoles (Nieuwkoop-Faber stage 54) were treated with TH (5nM T3) or dexamethasone (DEX, 2 uM), either separately or in combination, for 4 days. Lung cross-sections were then examined using hematoxylin-eosin histology, and immunohistochemically using an antibody against epithelial cadherin, and the actin-specific label, phalloidin. The appearance of e-cadherin-containing cells did not vary among treatments. However, compared with either untreated or DEX-treated tadpoles, the lung walls of tadpoles treated with TH-alone had significantly thicker cross-sections, more pronounced blood vessels, and a much higher proportion of actin-rich cells. Interestingly, DEX+TH lungs contained more actin than untreated or DEX-treated lungs, but less compared with TH-alone. These findings suggest that these two hormones exert different effects on lung development, with TH promoting the growth and/or proliferation of actin-containing cells in the lung, and GC inhibiting actin-containing cell development.