Differential β3 and β1 integrin expression in bone marrow and cortical bone of estrogen deficient rats
Voisin, Muriel C.
McNamara, Laoise M.
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Voisin, M. and McNamara, L. M. (2015), Differential β3 and β1 integrin expression in bone marrow and cortical bone of estrogen deficient rats. Anat. Rec., 298: 1548–1559. doi:10.1002/ar.23173
Integrin-based (beta(3)) attachments to the extracellular matrix (ECM) on osteocyte cell processes have recently been proposed to play an important role in facilitating osteocyte mechanosensation. However, it is not yet known whether integrin expression is altered in the mechanoregulatory osteocytes during osteoporosis. The objective of this study was to test the hypothesis that the expression of integrin-based mechanosensory complexes (beta(1) and beta(3) integrins) is altered as a direct response to estrogen deficiency, in an estrogen deficient animal model of osteoporosis. Four weeks post-operatively, immunohistochemistry was used to detect for beta(1) and beta(3) integrin subunits in bone tissue and marrow of ovariectomized (OVX; N-4) and SHAM (N-4) operated animals. A tartrate resistant acid phosphatase (TRAP) control stain was performed to quantify the presence of osteoclasts in the bone marrow and bone surfaces. Image analysis was performed to quantify expression patterns in different biological compartments, that is, bone marrow, endosteum, and cortical bone. Our results showed that beta(1) integrins were ubiquitously expressed throughout the bone and marrow, for both OVX and SHAM groups. beta(3) integrin subunit expression was lower in bone cells from osteoporotic animals compared to controls, whereas beta(3) expression in marrow cells did not differ significantly between groups. At the endosteum no difference was observed in beta(3) integrin subunit expression. As expected, the number of osteoclasts was higher in the OVX group validating an imbalance in bone remodeling. We propose that a reduction in beta(3) integrin expression in osteocytes might impair mechanosensation by bone cells during estrogen deficiency. (C) 2015 Wiley Periodicals, Inc.
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