TY - JOUR
T1 - Regulation of the mouse cellular retinoic acid-binding protein-I gene by thyroid hormone and retinoids in transgenic mouse embryos and P19 cells
AU - Wei, L. N.
AU - Lee, C. H.
AU - Filipcik, P.
AU - Chang, L.
PY - 1997/10
Y1 - 1997/10
N2 - The regulation of mouse cellular retinoic acid-binding protein-I (CRABP- I) gene expression by the retinoids and thyroid hormones was examined, by using a β-galactosidase (lacZ) reporter gene and a CRABP-I specific antibody, in transgenic mouse embryos and a mouse embryonal carcinoma cell line P19. The CRABP-lacZ reporter gene expression recapitulated the expression pattern of endogenous CRABP-I in the developing central nervous system. In mid-gestation mouse embryos the expression of both the transgene and the endogenous protein was elevated under the condition of hypovitaminosis A, suggesting that depletion of retinoic acid (RA) induced CRABP-I expression in embryos. Consistently, this reporter was suppressed by RA in P19 cells. In co-transfection experiments it was demonstrated that the expression of RARβ, RARγ or RXRα suppressed this reporter expression. In experiments designed to alter the thyroid hormone status in animals it was demonstrated that both the reporter gene and the endogenous CRABP-I expression were reduced by triiodothyronine injection and were elevated in a hypothyroidic condition induced by feeding with iodine-deficient diet supplemented with 6-propyl-2-thiouracil. In co-transfection experiments it was also demonstrated that the expression of T3Rβ suppressed the reporter expression in P19 cells. It was concluded that RA had a suppressive effect on CRABP-I gene expression in embryos and P19 cells and the effect could be mediated through RARβ, RARγ or RXRα. A role of thyroid hormones in CRABP- I gene expression and vitamin A metabolism in animals is discussed.
AB - The regulation of mouse cellular retinoic acid-binding protein-I (CRABP- I) gene expression by the retinoids and thyroid hormones was examined, by using a β-galactosidase (lacZ) reporter gene and a CRABP-I specific antibody, in transgenic mouse embryos and a mouse embryonal carcinoma cell line P19. The CRABP-lacZ reporter gene expression recapitulated the expression pattern of endogenous CRABP-I in the developing central nervous system. In mid-gestation mouse embryos the expression of both the transgene and the endogenous protein was elevated under the condition of hypovitaminosis A, suggesting that depletion of retinoic acid (RA) induced CRABP-I expression in embryos. Consistently, this reporter was suppressed by RA in P19 cells. In co-transfection experiments it was demonstrated that the expression of RARβ, RARγ or RXRα suppressed this reporter expression. In experiments designed to alter the thyroid hormone status in animals it was demonstrated that both the reporter gene and the endogenous CRABP-I expression were reduced by triiodothyronine injection and were elevated in a hypothyroidic condition induced by feeding with iodine-deficient diet supplemented with 6-propyl-2-thiouracil. In co-transfection experiments it was also demonstrated that the expression of T3Rβ suppressed the reporter expression in P19 cells. It was concluded that RA had a suppressive effect on CRABP-I gene expression in embryos and P19 cells and the effect could be mediated through RARβ, RARγ or RXRα. A role of thyroid hormones in CRABP- I gene expression and vitamin A metabolism in animals is discussed.
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U2 - 10.1677/joe.0.1550035
DO - 10.1677/joe.0.1550035
M3 - Article
C2 - 9390004
AN - SCOPUS:0030766348
SN - 0022-0795
VL - 155
SP - 35
EP - 46
JO - Journal of Endocrinology
JF - Journal of Endocrinology
IS - 1
ER -