-Microglobulin stimulates osteoclastic mediated bone mineral dissolution from neonatal mouse calvariae

Moe, Sharon M.; Barrett, Shean; Sprague, Stuart M.

doi:10.1016/0169-6009(92)91710-z

Cited by 5 publications

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“…23 The pathology appears to be specific to the osteoclast, as there is an absence of osteoblastic bone formation. 7 The subcutaneous injection of b 2 M induces histological evidence of bone resorption in neonatal mice, 8 and purified human b 2 M induces a dose-and time-dependent net calcium efflux in cultured murine calvariae (Figure 1; Moe and Sprague 9 and Moe et al 10 ). This calcium efflux has been shown to be mediated, in part, by IL-1b.…”

Section: Resultsmentioning

confidence: 99%

“…Subcutaneous injection of b 2 M induces histological evidence of bone resorption in neonatal mice, 8 and purified human b 2 M induces a dose-and time-dependent net calcium efflux in cultured murine calvariae. 9,10 This calcium efflux is mediated, in part, by interleukin-1b (IL-1b). 11 b 2 M also stimulates the synthesis of IL-6, a potent bone-resorbing cytokine, leading to increase in mRNA and protein levels in osteoblasts.…”

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confidence: 99%

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β2-Microglobulin stimulates osteoclast formation

Menaa

Esser

Sprague

2008

Kidney International

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Dialysis-related amyloidosis is a complication of long-term chronic kidney disease (CKD) resulting in deposition of beta(2)-microglobulin (beta(2)M) amyloid in osteoarticular tissue. Clinical manifestations include destructive arthropathy, bone cysts, and fractures. Since osteolytic lesions are prominent findings around the beta(2)M deposits, we sought evidence whether beta(2)M causes bone destruction by directly stimulating osteoclast activity and if this was mediated by local cytokine production. A dose-dependent increase in the number of tartrate-resistant alkaline phosphatase-positive multinucleated cells was found in cultured mouse marrow cells treated with beta(2)M. Osteoprotegerin was unable to block this osteoclastogenic effect of beta(2)M. Osteoblasts or stromal cells were not necessary to induce this osteoclastogenesis, as formation was induced by incubating beta(2)M with colony-forming unit granulocyte macrophages (the earliest identified precursor of osteoclasts) or the murine RAW 264.7 monocytic cell line. beta(2)M Upregulated tumor necrosis factor-alpha (TNF-alpha) and IL-1 expression in a dose-dependent manner; however, a TNF-alpha-neutralizing antibody blocked beta(2)M-induced osteoclast formation. These results show that beta(2)M stimulates osteoclastogenesis, supporting its direct role in causing bone destruction in patients with CKD.

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Section: Resultsmentioning

confidence: 99%

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confidence: 99%

β2-Microglobulin stimulates osteoclast formation

Menaa

Esser

Sprague

2008

Kidney International

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“…Although the effect of β 2 M on osteoblast proliferation is controversial, multiple other effects of β 2 M on bone cell metabolism have been observed. Subcutaneous injection of β 2 M induces histologic evidence of bone resorption in neonatal mice (12), and purified human β 2 M induces a dose‐ and time‐dependent net calcium efflux in cultured murine calvaria (11, 13). This calcium efflux is mediated, in part, by interleukin (IL)‐1β(14).…”

Section: β2m As a Bone‐resorbing Agentmentioning

confidence: 99%

“…Dialysis‐related amyloidosis (DRA), also referred to as β 2 ‐microglobulin amyloidosis (Aβ 2 M), is most commonly seen in patients with end‐stage renal disease (ESRD) undergoing long‐term hemodialysis therapy (13). However, it also occurs among patients undergoing chronic peritoneal dialysis and prior to initiation of dialytic therapy (1, 4).…”

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The Pathogenesis of β₂‐Microglobulin–Induced Bone Lesions in Dialysis‐Related Amyloidosis

Tran

Rutecki

Sprague

2001

Seminars in Dialysis

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Dialysis-related amyloidosis (DRA), also referred to as beta(2)-microglobulin amyloidosis (A beta(2)M), is an important cause of morbidity in patients with chronic renal failure and in those who are on dialysis. Although DRA deposits from affected joints have been characterized as a unique amyloid fibril protein, beta(2)M, less is known about the pathologic role of beta(2)M as a mediator of bone and joint disease. Potential mechanisms for beta(2)M pathologic interaction in bone include bone growth factors, cytokines, and advanced glycation end products (AGEs). It appears that DRA is the result of a complex interaction between bone resorption and surrounding tissue destruction culminating in beta(2)M deposition and amyloid formation. More work is required to elucidate the relationship between beta(2)M accumulation and progressive tissue destruction.

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“…Serum β 2 M has been suggested to be a marker of bone remodeling in postmenopausal women (14, 15). It has been shown that β 2 M causes cytokine‐mediated bone resorption in DRA (16–18). However, the mechanism of β 2 M action on bone cells is not certain, since there is no known receptor for β 2 M.…”

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Role of β₂‐Microglobulin in the Immune Response in Renal Osteodystrophy

Bálint

2001

Seminars in Dialysis

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Renal osteodystrophy is the major cause of skeletal morbidity in dialysis patients. It is characterized by beta(2)-microglobulin (beta(2)M) amyloid deposition at the osteoarticular sites and a destructive arthropathy. beta(2)M is present on the surface of all nucleated cells as the small extracellular subunit of the major histocompatibility complex (MHC) class I molecule and actively participates in the immune response. Accumulating evidence suggests that beta(2)M plays a key role in the development of renal osteodystrophy through a T cell-mediated inflammatory immune mechanism.

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-Microglobulin stimulates osteoclastic mediated bone mineral dissolution from neonatal mouse calvariae

Cited by 5 publications

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β2-Microglobulin stimulates osteoclast formation

β2-Microglobulin stimulates osteoclast formation

The Pathogenesis of β₂‐Microglobulin–Induced Bone Lesions in Dialysis‐Related Amyloidosis

Role of β₂‐Microglobulin in the Immune Response in Renal Osteodystrophy

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-Microglobulin stimulates osteoclastic mediated bone mineral dissolution from neonatal mouse calvariae

Cited by 5 publications

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β2-Microglobulin stimulates osteoclast formation

β2-Microglobulin stimulates osteoclast formation

The Pathogenesis of β2‐Microglobulin–Induced Bone Lesions in Dialysis‐Related Amyloidosis

Role of β2‐Microglobulin in the Immune Response in Renal Osteodystrophy

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The Pathogenesis of β₂‐Microglobulin–Induced Bone Lesions in Dialysis‐Related Amyloidosis

Role of β₂‐Microglobulin in the Immune Response in Renal Osteodystrophy