RETINYL ESTER STORAGE IS NORMAL IN TRANSGENIC MICE WITH ENHANCED EXPRESSION OF CELLULAR RETINOL-BINDING PROTEIN TYPE-I

This report describes the production and characterization of transgeni c mice with high expression of human cellular retinol-binding protein type I [hCRBP(I)]. In initial experiments, overexpression of hCRBP(I) was driven by the strong promoter SR alpha, but no transgenic offsprin g were produced. When we used the less efficient mouse metallothionein I promoter fused to the hCRBP(I) cDNA for microinjection, we obtained 12% transgenic offspring. Two of these transgenic mice (409/1 and 401 /2) expressed mRNA and immunoreactive hCRBP(I) in several organs. Both lines had relatively high contents of hCRBP(I) in intestine, testis a nd epididymis. On the other hand, only 401/2 transgenic mice had high contents of hCRBP(I) in kidney. Effects on storage of vitamin A were s tudied by measuring the concentration of retinyl esters in different o rgans. The concentrations of retinyl esters in liver, lung and kidney aid not significantly differ between transgenic and control mice, and the concentration of total retinol in plasma was within the normal ran ge in transgenic mice. Furthermore, feeding mice a diet with high or l ow concentrations of vitamin A for 2 wks resulted in no marked differe nces in the concentrations of retinyl esters in liver, kidney, lung, i ntestine and testis in transgenic mice compared with control mice. The refore, in spite of high expression of hCRBP(I) in several organs, the transgenic mice had normal storage of retinyl esters in all organs st udied. The present in vivo study indicates that the CRBP(I) content al one does not control retinyl ester storage.