The hydrocortisone-induced transcriptional down-regulation of beta-galactoside alpha2,6-sialyltransferase in the small intestine of suckling rats is suppressed by mifepristone (RU-38.486).
The progressive loss of sialic acids of the brush-border membrane glycoproteins is one of the major biochemical changes which occur in the rat small intestine during the transition from suckling to weaning, and this process is speeded up by an injection of glucocorticoids to the suckling animals. We used the rat liver beta-galactoside alpha2,6-sialyltransferase (ST6(N), EC 2.4.99.1) cDNA as a probe to examine the mRNA level of this enzyme in the small intestine of both suckling (13-day-old) and weaned (25-day-old) rats. In the ileum of suckling rats, the ST6(N) mRNA level was about four times higher than in the jejunum, whereas the membrane-bound enzyme activity was less than two times higher. In comparison with the controls, hydrocortisone treatment significantly decreased the level of this transcript and of the corresponding enzyme activity in both segments of the small intestine of suckling rats. Additionally, the antiglucocorticoid mifepristone (RU-38.486) suppressed the effect of hydrocortisone. The expression of ST6(N) mRNA in the small intestine of weaned (25-day-old) rats was several times lower than that in suckling (13-day-old) rats, and was unresponsive to hydrocortisone as well as to mifepristone. These results indicate that the glucocorticoid-induced transcriptional down-regulation of ST6(N) expression in the small intestine of suckling rats is mediated via the glucocorticoid receptor pathway, and support the notion that alterations in sialylation of brush-border membrane glycoconjugates occurring upon weaning are the result of a lower expression of ST6(N).
Hamr
A
A
Institute of Physiology, Academy of Sciences of the Czech Republic, Prague.
Delannoy
P
P
Verbert
A
A
Kolínská
J
J
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D002462:Cell Membrane / Q000187:drug effects / Q000201:enzymology; D015536:Down-Regulation; D005260:Female; D006727:Hormone Antagonists / Q000494:pharmacology; D006854:Hydrocortisone / Q000494:pharmacology*; D007082:Ileum / Q000187:drug effects / Q000201:enzymology; D007413:Intestinal Mucosa / Q000201:enzymology; D007421:Intestine, Small / Q000187:drug effects / Q000201:enzymology*; D007583:Jejunum / Q000187:drug effects / Q000201:enzymology; D008871:Microvilli / Q000187:drug effects / Q000201:enzymology; D015735:Mifepristone / Q000494:pharmacology*; D011247:Pregnancy; D012333:RNA, Messenger / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011965:Receptors, Glucocorticoid / Q000187:drug effects / Q000378:metabolism; D012799:Sialyltransferases / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism; D012995:Solubility; D013391:Sucking Behavior / Q000187:drug effects*; D014158:Transcription, Genetic / Q000187:drug effects; D014886:Weaning; D000094802:beta-D-Galactoside alpha 2-6-Sialyltransferase
D000893:Anti-Inflammatory Agents; D006727:Hormone Antagonists; D012333:RNA, Messenger; D011965:Receptors, Glucocorticoid; D015735:Mifepristone; D012799:Sialyltransferases; D006854:Hydrocortisone; D000094802:beta-D-Galactoside alpha 2-6-Sialyltransferase