Trehalase gene expression during postnatal development of rabbit intestine and kidney: effects of glucocorticoids

Abstract

Rabbit trehalase is a 75-kDa glycosyl phosphatidylinositol-anchored glycoprotein of the microvillus membrane of the enterocyte and kidney proximal tubule epithelial cells. The purpose of this work was to try to elucidate the molecular basis of trehalase gene expression in intestine and kidney during normal postnatal development and after hydrocortisone injection in suckling rabbits. Trehalase cDNA isolated, sequenced, and characterized by J. Ruf, H. Wacker, P. James. M. Maffia, P. Seiler, G. Galand, A. Kieckebusch, G. Semenza, and N. Mantei (J. Biol. Chem. 265: 15034-15039, 1990) was used to quantify trehalase mRNA. To measure the amount of trehalase mRNA encoding for trehalase, poly(A)+ mRNA was isolated and analyzed by Northern blot hybridization. This cDNA hybridized to a 1.8-kb mRNA in the small intestine and kidney. In developing rabbit intestine, after a slow decrease between 4 and 10 days, there is a sharp and parallel rise of both trehalase specific activity (28x) and mRNA (10x) between 10 and 30 days after birth. In contrast, in the kidney, between 4 and 30 days, the general developmental profile of both parameters is very different. There is an overall significant and parallel increase of both trehalase specific activity (3.3x) and mRNA (4.3x). In intestine the longitudinal gradient of trehalase activity and mRNA expression is different in adult and 16-day cortisol-treated suckling rabbits. In intestine, between 10 and 14 days, cortisol induces a coordinate increase of both trehalase activity (26x) and mRNA (19x), but at 16 days the two parameters diverge markedly. Daily injections of cortisol between 10 and 16 days do not induce significantly trehalase mRNA over controls at 16 days. In only 2 days, between 14 and 16 days, there is a clear loss of trehalase mRNA responsiveness to glucocorticoids. On the contrary, in the kidney, daily injections of cortisol between 10 and 16 days have no significant effect on trehalase mRNA but induce a small and significant increase of trehalase specific activity at 16 days (1.8x). Therefore we conclude that, with respect to the distribution along the small intestine, normal development in kidney and intestine, and after induction with glucocorticoid in intestine, alteration in the steady-state levels of trehalase mRNA is a major mechanism for the regulation of trehalase gene expression.