期刊
JOURNAL OF CELLULAR BIOCHEMISTRY
卷 109, 期 5, 页码 927-932出版社
WILEY-BLACKWELL
DOI: 10.1002/jcb.22468
关键词
MEGAKARYOCYTES; OSTEOBLASTS; INTEGRINS; CD41; IL-3
资金
- NIH/NAIMS [AR47342, AR055269, AR46032]
- Department of Orthopaedics and Rehabilitation at Yale University School of Medicine
- Department of Orthopaedic Surgery at Indiana University School of Medicine
As the prevalence of osteoporosis is expected to increase over the next few decades, the development of novel therapeutic strategies to combat this disorder becomes clinically imperative. These efforts draw extensively from an expanding body of knowledge pertaining to the physiologic mechanisms of skeletal homeostasis. To this body of knowledge, we contribute that cells of hematopoietic lineage may play a crucial role in balancing osteoblastic bone formation against osteoclastic resorption. Specifically, our laboratory has previously demonstrated that megakaryocytes (MKs) can induce osteoblast (OB) proliferation in vitro, but do so only when direct cell-to-cell contact is permitted. To further investigate the nature of this interaction, we have effectively neutralized several adhesion molecules known to function in the analogous interaction of MKs with another cell type of mesenchymal origin the fibroblast (FB). Our findings implicate the involvement of fibronectin/RGD-binding integrins including alpha 3 beta 1 (VLA-3) and alpha 5 beta 1 (VLA-5) as well as glycoprotein (gp) IIb (CD41), all of which are known to be expressed on MK membranes. Furthermore, we demonstrate that interleukin (IL)-3 can enhance MK-induced OB activation in vitro, as demonstrated in the MK-FB model system. Taken together, these results suggest that although their physiologic and clinical implications are very different, these two models of hematopoietic-mesenchymal cell activation are mechanistically analogous in several ways. J. Cell. Biochem. 109: 927-932, 2010. (C) 2010 Wiley-Liss, Inc.
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