期刊
JOURNAL OF BONE AND MINERAL METABOLISM
卷 27, 期 1, 页码 16-23出版社
SPRINGER JAPAN KK
DOI: 10.1007/s00774-008-0012-z
关键词
Myeloma; Osteoclast; Stromal cell; MIP-1; VLA-4
资金
- Scientific Research (A)
- Ministry of Education, Culture, Science, and Sports of Japan
- Ministry of Health, Labor, and Welfare of Japan
Multiple myeloma (MM) cell adhesion to stromal cells via very late antigen (VLA)-4 and vascular cell adhesion molecule (VCAM)-1 interaction causes enhanced secretion of osteoclastogenic activity by MM cells. We have reported that MM cell-derived macrophage inflammatory protein (MIP)-1 alpha and MIP-1 beta are responsible for most of the osteoclastogenic activity in MM. Thus, adhesion-mediated osteoclastogenesis may be caused by enhanced production of MIP-1 via VLA-4-VCAM-1 interaction. The present study was undertaken to clarify whether MM cell-derived MIP-1 plays a role in VLA-4-VCAM-1 adhesion-mediated osteoclastogenesis. Adhesion of MM cells to VCAM-1 upregulated MIP-1 alpha and MIP-1 beta production from MM cells and enhanced production of osteoclastogenic activity by MM cells. Blockade of MIP-1 alpha and MIP-1 beta actions not only abrogated elaboration of osteoclastogenic activity, but also suppressed spontaneous MM cell adhesion to VCAM-1. These results demonstrate that MM cell adhesion to VCAM-1 upregulates MIP-1 production by MM cells to cause enhancement of osteoclastogenesis. In addition, the results suggest that the increased production of MIP-1 further enhances MM cell binding to stromal cells via stimulation of VLA-4-VCAM-1 adhesion, forming a vicious cycle between MM cell adhesion to stromal cells and MIP-1 production via VLA-4-VCAM-1 interaction.
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