Macrophage inflammatory protein 1-alpha is a potential osteoclast stimulatory factor in multiple myeloma

Sun Jin Choi, Jose C. Cruz, Fiona Craig, Hoyeon Chung, Rowena D. Devlin, G. David Roodman, Melissa Alsina

Research output: Contribution to journalArticle

322 Citations (Scopus)

Abstract

This study was designed to determine if macrophage inhibitory protein- 1α (MIP-1α), a recently described osteoclast (OCL) stimulatory factor, was present in marrow from patients with multiple myeloma (MM) and possibly involved in the bone destructive process. MIP-1α, but not interleukin-1β (IL-1β), tumor necrosis factor-β (TNF-β), or interleukin-6 (IL-6), messenger RNA was elevated in freshly isolated bone marrow from 3 of 4 patients with MM compared to normal controls. Furthermore, enzyme-linked immunosorbent assays of freshly isolated bone marrow plasma detected increased concentrations of hMIP-α (range, 75-7784 pg/mL) in 8 of 13 patients (62%) with active myeloma, in 3 of 18 patients (17%) with stable myeloma (range, 75-190.3), as well as in conditioned media from 4 of 5 lymphoblastoid cell lines (LCLs) derived from patients with MM. Mildly elevated levels of MIP-1α were detected in 3 of 14 patients (21%) with other hematologic diagnoses (range, 80.2-118.3, median value of 96 pg/mL) but not in normal controls (0 of 7). MIP-1α was not detected in the peripheral blood of any patients with MM. In addition, recombinant hMIP-1α induced OCL formation in human bone marrow cultures. Importantly, addition of a neutralizing antibody to MIP-1α to human bone marrow cultures treated with freshly isolated marrow plasma from patients with MM blocked the increased OCL formation induced by these marrow samples but had no effect on control levels of OCL formation. Thus, high levels of MIP-1α are expressed in marrow samples from patients with MM, but not in marrow from patients with other hematologic disorders or controls, and support an important role for MIP-1α as one of the major factors responsible for the increased OCL stimulatory activity in patients with active MM. (C) 2000 by The American Society of Hematology.

Original languageEnglish (US)
Pages (from-to)671-675
Number of pages5
JournalBlood
Volume96
Issue number2
StatePublished - Jul 15 2000
Externally publishedYes

Fingerprint

Chemokine CCL3
Macrophages
Osteoclasts
Multiple Myeloma
Bone Marrow
Bone
Proteins
Plasmas
Immunosorbents
Level control
Conditioned Culture Medium
Neutralizing Antibodies
Interleukin-1
Cell culture
Interleukin-6
Assays
Blood
Tumor Necrosis Factor-alpha
Cells
Messenger RNA

ASJC Scopus subject areas

  • Hematology

Cite this

Choi, S. J., Cruz, J. C., Craig, F., Chung, H., Devlin, R. D., Roodman, G. D., & Alsina, M. (2000). Macrophage inflammatory protein 1-alpha is a potential osteoclast stimulatory factor in multiple myeloma. Blood, 96(2), 671-675.

Macrophage inflammatory protein 1-alpha is a potential osteoclast stimulatory factor in multiple myeloma. / Choi, Sun Jin; Cruz, Jose C.; Craig, Fiona; Chung, Hoyeon; Devlin, Rowena D.; Roodman, G. David; Alsina, Melissa.

In: Blood, Vol. 96, No. 2, 15.07.2000, p. 671-675.

Research output: Contribution to journalArticle

Choi, SJ, Cruz, JC, Craig, F, Chung, H, Devlin, RD, Roodman, GD & Alsina, M 2000, 'Macrophage inflammatory protein 1-alpha is a potential osteoclast stimulatory factor in multiple myeloma', Blood, vol. 96, no. 2, pp. 671-675.
Choi SJ, Cruz JC, Craig F, Chung H, Devlin RD, Roodman GD et al. Macrophage inflammatory protein 1-alpha is a potential osteoclast stimulatory factor in multiple myeloma. Blood. 2000 Jul 15;96(2):671-675.
Choi, Sun Jin ; Cruz, Jose C. ; Craig, Fiona ; Chung, Hoyeon ; Devlin, Rowena D. ; Roodman, G. David ; Alsina, Melissa. / Macrophage inflammatory protein 1-alpha is a potential osteoclast stimulatory factor in multiple myeloma. In: Blood. 2000 ; Vol. 96, No. 2. pp. 671-675.
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abstract = "This study was designed to determine if macrophage inhibitory protein- 1α (MIP-1α), a recently described osteoclast (OCL) stimulatory factor, was present in marrow from patients with multiple myeloma (MM) and possibly involved in the bone destructive process. MIP-1α, but not interleukin-1β (IL-1β), tumor necrosis factor-β (TNF-β), or interleukin-6 (IL-6), messenger RNA was elevated in freshly isolated bone marrow from 3 of 4 patients with MM compared to normal controls. Furthermore, enzyme-linked immunosorbent assays of freshly isolated bone marrow plasma detected increased concentrations of hMIP-α (range, 75-7784 pg/mL) in 8 of 13 patients (62{\%}) with active myeloma, in 3 of 18 patients (17{\%}) with stable myeloma (range, 75-190.3), as well as in conditioned media from 4 of 5 lymphoblastoid cell lines (LCLs) derived from patients with MM. Mildly elevated levels of MIP-1α were detected in 3 of 14 patients (21{\%}) with other hematologic diagnoses (range, 80.2-118.3, median value of 96 pg/mL) but not in normal controls (0 of 7). MIP-1α was not detected in the peripheral blood of any patients with MM. In addition, recombinant hMIP-1α induced OCL formation in human bone marrow cultures. Importantly, addition of a neutralizing antibody to MIP-1α to human bone marrow cultures treated with freshly isolated marrow plasma from patients with MM blocked the increased OCL formation induced by these marrow samples but had no effect on control levels of OCL formation. Thus, high levels of MIP-1α are expressed in marrow samples from patients with MM, but not in marrow from patients with other hematologic disorders or controls, and support an important role for MIP-1α as one of the major factors responsible for the increased OCL stimulatory activity in patients with active MM. (C) 2000 by The American Society of Hematology.",
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