Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 264, Issue 1-2, Pages 164-170Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2006.11.006
Keywords
glucocorticoids; chondrocytes; growth plate; proliferation
Categories
Funding
- Biotechnology and Biological Sciences Research Council [BBS/E/R/00000682] Funding Source: researchfish
- Biotechnology and Biological Sciences Research Council [BBS/E/R/00000682] Funding Source: Medline
Ask authors/readers for more resources
Long-term use of glucocorticoids (GC) can cause growth retardation in children due to their actions on growth plate chondrocytes. AL-438, a nonsteroidal anti-inflammatory agent that acts through the glucocorticoid receptor (GR) retains full anti-inflammatory efficacy but has reduced negative effects on ostcoblasts compared to those elicited by prednisolone (Pred) or dexamethasone (Dex). We have used the murine chondrogenic ATDC5 cell line to compare the effects of AL-438 with those of Dex and Pred on chondrocyte dynamics. Dex and Pred caused a reduction in cell proliferation and proteoglycan synthesis, whereas exposure to AL-438 had no effect. LPS-induced IL-6 production in ATDC5 cells was reduced by Dex or AL-438, showing that AL-438 has similar anti-inflammatory efficacy to Dex in these cells. Fetal mouse metatarsals grown in the presence of Dex were shorter than control bones whereas AL-438 treated metatarsals paralleled control bone growth. These results indicate that the adverse effects Dex or Pred have on chondrocyte proliferation and bone growth were attenuated following AL-438 exposure, suggesting that AL-438 has a reduced side effect profile on chondrocytes compared to other GCs. This could prove important in the search for new anti-inflammatory treatments for children. (c) 2006 Elsevier Ireland Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available