Thyroid hormone and its receptors and metabolizing enzymes contribute to the regulation of carbonic anhydrase expression in neural retina
Por:
Peterson R.E., Orozco A., Linser P.J.
Publicada:
1 ene 1996
Resumen:
Purpose. The goal of this study was to assess the role of the thyroid hormone system in regulating the expression of carbonic anhydrase-II at various stages of neural retina development. Methods. Standard immunochemical, biochemical and molecular biological methods were used to measure the levels of thyroid hormone receptor ?(C-erbA), thyronine metabolizing enzyme Type II 5?-deiodinase and how these correlate with changes in expression of carbonic anhydrase-II as functions of chick retina development. Cultured embryonic retina cells were also used to measure the effects of the depletion and/or addition of thyroid hormone on carbonic anhydrase mRNA concentration (Northern analysis). Results. As previously reported by others (Sjoberg et al, Development 114:39-47, 1992), C-erbA is present continuously in retina from early in development into maturity. Immunohistochemistry showed the protein to be present in many retinal cells including Müller glial cells. The activity of Type II 5?-deiodinase (the enzyme necessary for local activation of T4 into T3) showed a developmental pattern of increase-decrease-increase that mimics the pattern for carbonic anhydrase-II expression. Culture of embryonic retina cells in the absence of T3 reduces carbonic anhydrase [mRNA] while addition of exogenous T3 induces higher levels of expression. Conclusions. These results are consistent with the hypothesis that Thyroid hormone plays a role in the regulation of carbonic anhydrase expression in the embryonic neural retina. Nevertheless, depletion of T3 from the environment of retina cells failed to abolish carbonic anhydrase expression and therefore it is likely that multiple factors are involved in the regulation of expression of this highly concentrated retinal enzyme. Ongoing analyses of the carbonic anhydrase promoter are consistent with a multi-factorial regulatory scheme.
Filiaciones:
Peterson R.E.:
Whitney Laboratory, Dept. of Anatomy and Cell Biology, University of Florida
Orozco A.:
Departmento de Fisiologia, UNAM, Mexico D.F., Mexico
Linser P.J.:
Whitney Laboratory, Dept. of Anatomy and Cell Biology, University of Florida
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