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Blood, 1 June 2001, Vol. 97, No. 11, pp. 3349-3353
CHEMOKINES
Macrophage inflammatory protein-1 is an osteoclastogenic
factor in myeloma that is independent of receptor activator of nuclear
factor  B ligand
Je-Ho Han,
Sun Jin Choi,
Noriyoshi Kurihara,
Masanori Koide,
Yasuo Oba, and
G. David Roodman
From the Department of Medicine/Hematology, University
of Texas Health Science Center, San Antonio, and the General Clinical
Research Center and Research Service of the Audie L. Murphy Veterans
Administration Hospital, San Antonio, Texas.
A complementary DNA expression library derived from marrow samples
from myeloma patients was recently screened and human macrophage inflammatory protein-1 (hMIP-1) was identified as an
osteoclastogenic factor expressed in these samples. hMIP-1 enhanced
osteoclast (OCL) formation in human marrow cultures and by highly
purified OCL precursors in a dose-dependent manner (5-200 pg/mL).
Furthermore, hMIP-1 enhanced OCL formation induced by human
interleukin-6 (IL-6), which is produced by marrow stromal cells when
they interact with myeloma cells. hMIP-1 also enhanced OCL formation
induced by parathyroid hormone-related protein (PTHrP) and receptor
activator of nuclear factor  B ligand (RANKL), factors also
implicated in myeloma bone disease. Time-course studies revealed that
the hMIP-1 acted during the last 2 weeks of the 3-week culture
period. Reverse transcription-polymerase chain reaction analysis
showed that the chemokine receptors for hMIP-1 (CCR1 and CCR5) were
expressed by human bone marrow and highly purified early OCL
precursors. Furthermore, hMIP-1 did not increase expression of
RANKL. These data demonstrate that hMIP-1 is an osteoclastogenic
factor that appears to act directly on human OCL progenitors and acts
at the later stages of OCL differentiation. These data further suggest that in patients with myeloma, MIP-1 produced by myeloma cells, in
combination with RANKL and IL-6 that are produced by marrow stromal
cells in response to myeloma cells, enhances OCL formation through
their combined effects on OCL precursors.
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