EXPRESSION OF RETINOIC ACID NUCLEAR RECEPTORS AND TISSUE TRANSGLUTAMINASE IS ALTERED IN VARIOUS TISSUES OF RATS FED A VITAMIN-A-DEFICIENT DIET

被引:78
作者
VERMA, AK [1 ]
SHOEMAKER, A [1 ]
SIMSIMAN, R [1 ]
DENNING, M [1 ]
ZACHMAN, RD [1 ]
机构
[1] UNIV WISCONSIN, DEPT PEDIAT, MADISON, WI 53792 USA
关键词
RATS; RETINOIC ACID NUCLEAR RECEPTORS; TISSUE TRANSGLUTAMINASE; GENE EXPRESSION; VITAMIN-A DEFICIENCY;
D O I
10.1093/jn/122.11.2144
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
The effects of vitamin A nutritional status on the levels of expression of retinoic acid nuclear receptors (RAR), and the retinoic acid-responsive gene, tissue transglutaminase, were determined in rats. Weanling male Sprague-Dawley rats fed a vitamin A-deficient diet for approximately 7 wk developed vitamin A deficiency, as confirmed by the depletion of liver retinol and retinyl palmitate. Controls were fed the same diet supplemented with 24 mg/kg retinyl acetate. The levels of expression of RARbeta mRNA were approximately 80% lower in bladder, brain, liver, lung and trachea and those of RARgamma mRNA were approximately 50% lower in bladder, lung and trachea of rats fed the vitamin A-deficient diet than in controls. The levels of expression of RARalpha mRNA were approximately 90% lower in brain and approximately 30% greater in liver, kidney, intestine and lung of rats fed the vitamin A-deficient diet. Vitamin A deficiency also resulted in reduced expression of tissue transglutaminase in the bladder, lungs and trachea, which paralleled the effects observed for RARbeta and RARgamma. When vitamin A-deficient rats were subsequently fed a retinol-deficient diet supplemented with retinoic acid for 4 wk, the expression of RAR (beta and gamma) and tissue transglutaminase returned to the control levels. These results indicate that vitamin A nutritional status in rats influences the expression of both RAR and tissue transglutaminase in certain tissues.
引用
收藏
页码:2144 / 2152
页数:9
相关论文
共 43 条
[1]  
BLANER WS, 1986, J LIPID RES, V27, P1084
[2]   IDENTIFICATION OF A 2ND HUMAN RETINOIC ACID RECEPTOR [J].
BRAND, N ;
PETKOVICH, M ;
KRUST, A ;
CHAMBON, P ;
DETHE, H ;
MARCHIO, A ;
TIOLLAIS, P ;
DEJEAN, A .
NATURE, 1988, 332 (6167) :850-853
[3]   MORPHOGENS IN CHICK LIMB DEVELOPMENT [J].
BRICKELL, PM ;
TICKLE, C .
BIOESSAYS, 1989, 11 (05) :145-149
[4]   REGULATION OF TISSUE TRANSGLUTAMINASE GENE-EXPRESSION AS A MOLECULAR-MODEL FOR RETINOID EFFECTS ON PROLIFERATION AND DIFFERENTIATION [J].
CHIOCCA, EA ;
DAVIES, PJA ;
STEIN, JP .
JOURNAL OF CELLULAR BIOCHEMISTRY, 1989, 39 (03) :293-304
[5]  
CHOMCZYNSKI P, 1987, ANAL BIOCHEM, V162, P156, DOI 10.1016/0003-2697(87)90021-2
[6]  
De Luca L M, 1985, Acta Vitaminol Enzymol, V7 Suppl, P13
[7]  
DE LUCA LM, 1991, FASEB J, V5, P2924
[8]  
DELUCA HF, 1979, FED PROC, V38, P2519
[9]   INVOLVEMENT OF RETINOIC ACID NUCLEAR RECEPTORS IN RETINOIC ACID-INDUCED TISSUE TRANSGLUTAMINASE GENE-EXPRESSION IN RAT TRACHEAL 2C5 CELLS [J].
DENNING, MF ;
VERMA, AK .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1991, 175 (01) :344-350
[10]   IDENTIFICATION OF A RETINOIC ACID RESPONSIVE ELEMENT IN THE RETINOIC ACID RECEPTOR-BETA GENE [J].
DETHE, H ;
VIVANCORUIZ, MD ;
TIOLLAIS, P ;
STUNNENBERG, H ;
DEJEAN, A .
NATURE, 1990, 343 (6254) :177-180