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Osteopontin is associated with nuclear factor kappaB gene expression during tail-suspension-induced bone loss.

Abstract：

:Osteoporosis due to unloading-induced bone loss is a critical issue in the modern aging society. Although the mechanisms underlying this phenomenon are largely unknown, osteopontin (OPN) is one of the critical mediators required for unloading-induced bone loss [M. Ishijima, S.R. Rittling, T. Yamashita, K. Tsuji, H. Kurosawa, A. Nifuji, D.T. Denhardt, and M. Noda, Enhancement of osteoclastic bone resorption and suppression of osteoblastic bone formation in response to reduced mechanical stress do not occur in the absence of osteopontin, J Exp Med, 193 (2001) 399-404]. To clarify the molecular bases for OPN actions, we carried out microarray analyses on the genes expressed in the femoral bone marrow cells in wild type and OPN-/- mice. The removal of the mechanical load induced bone loss in wild type, but not in OPN-/- mice, as previously reported. Expression analysis of 9586 cDNAs on a microarray system revealed that OPN deficiency blocked tail-suspension-induced expression of ten genes (group A). This observation was confirmed based on semi-quantitative RT-PCR analyses. On the other hand, expression of four genes (group B) was not altered by tail suspension in wild type but was enhanced in OPN-deficient mice. NF-kappaB p105 subunit gene (Nfkb1) was found in group A and Bax in group B. p53 gene expression was upregulated by tail suspension in wild type mice, but it was no longer observed in OPN-/- mice. These data indicate that OPN acts to mediate mechanical stress signaling upstream to the genes encoding apoptosis-related molecules, and its action is associated with alteration of the genes.

journal_name

Exp Cell Res

journal_title

Experimental cell research

authors

Ishijima M,Ezura Y,Tsuji K,Rittling SR,Kurosawa H,Denhardt DT,Emi M,Nifuji A,Noda M

doi

10.1016/j.yexcr.2006.06.003

subject

Has Abstract

pub_date

2006-10-01 00:00:00

pages

3075-83

issue

16

eissn

0014-4827

issn

1090-2422

pii

S0014-4827(06)00219-9

journal_volume

312

pub_type

杂志文章

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