| Autor: |
Pandipati S; Department of Periodontics, Prevention, and Geriatrics, School of Dentistry, University of Michigan, Ann Arbor 48109-1078, USA., Driscoll JE, Franceschi RT |
| Jazyk: |
angličtina |
| Zdroj: |
Journal of cellular physiology [J Cell Physiol] 1998 Jul; Vol. 176 (1), pp. 85-91. |
| DOI: |
10.1002/(SICI)1097-4652(199807)176:1<85::AID-JCP10>3.0.CO;2-N |
| Abstrakt: |
Ascorbic acid (AA) is an essential cofactor for osteoblast differentiation both in vivo and in vitro. Before it can function, this vitamin must be transported into cells via a specific Na+-dependent AA transporter. In this study, we examine the regulation of this transport activity by glucocorticoids, a class of steroid hormones known to stimulate in vitro osteoblast differentiation. Dexamethasone stimulated Na+-dependent AA transport activity approximately twofold in primary rat calvarial osteoblasts. Effects of hormone on ascorbic acid transport were rapid (detected within 24 h) and were maximally stimulated by 25-50 nM dexamethasone. Similar effects of dexamethasone on transport activity were also observed in murine MC3T3-E1 cells. This preosteoblast cell line was used for a more detailed characterization of the glucocorticoid response. Transport activity was stimulated selectively by glucocorticoids (dexamethasone > corticosterone) relative to other steroid hormones (progesterone and 17-beta-estradiol) and was blocked when cells were cultured in the presence of cycloheximide, a protein synthesis inhibitor. Kinetic analysis of AA transporter activity in control and dexamethasone-treated cells indicated a Km of approximately 17 microM for both groups. In contrast, dexamethasone increased Vmax by approximately 2.5-fold. Cells also contained an Na+-independent glucose transport activity that has been reported in other systems to transport vitamin C as oxidized dehydroascorbic acid. In marked contrast to Na+-dependent AA transport, this activity was inhibited by dexamethasone. Thus, glucocorticoids increase Na+-dependent AA transport in osteoblasts, possibly via up-regulation of transporter synthesis, and this response can be resolved from actions of glucocorticoids on glucose transport. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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