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Retinoic acid stimulates expression of the functional osteoclast integrin α v β 3 : Transcriptional activation of the β 3 but not the α v gene
Author(s) -
Chiba Mirei,
Teitelbaum Steven L.,
Cao Xu,
Ross F. Patrick
Publication year - 1996
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/(sici)1097-4644(19960915)62:4<467::aid-jcb4>3.0.co;2-k
Subject(s) - retinoic acid , integrin , osteoclast , microbiology and biotechnology , retinoic acid inducible orphan g protein coupled receptor , gene expression , gene , chemistry , biology , retinoic acid receptor , genetics , cell , receptor
The capacity of osteoclasts to resorb bone depends, in part, on the surface expression of the integrin α v β 3 . We have investigated whether the steroid hormone retinoic acid, known to stimulate bone resorption, regulates the appearance of the α v β 3 complex in avian osteoclast presursors. Using surface labeling, followed by immunoprecipitation with a α v β 3 ‐specific antibody, we show that retinoic acid increases surface expression of the heterodimer in a dose‐ and time‐dependent manner. Northern analysis reveals that the high basal steady‐state levels of α v mRNA do not change, while those for β 3 rise significantly from their initially low levels. Nuclear run‐on studies confirm that steroid treatment stimulates transcription of the β 3 , but not the α v gene. Osteoclast precursors treated with retinoic acid exhibit increased multinucleation and expression of the osteoclast marker enzyme tartrate‐resistant acid phosphatase. However, the fused cells do not have an increased capacity to resorb bone. In summary, multinucleated cells generated in this study do not represent fully differentiated bone‐resorbing polykaryons. These results suggest that treatment of osteoclast precursors with retinoic acid is necessary, but insufficient, for expression of the mature osteoclast phenotype. © 1996 Wiley‐Liss, Inc.