Activation of the bone-derived latent TGF beta complex by isolated osteoclasts

Oreffo, Richard O.C.; Mundy, Gregory R.; Seyedin, Saeid M.; Bonewald, Lynda F.

doi:10.1016/0006-291x(89)92795-2

Cited by 272 publications

(125 citation statements)

References 13 publications

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“…LAP regulates TGF-,B activity in cell culture (Gentry and Nash, 1990) and in vivo (Wallick et al, 1990) and influences the distribution of TGF-,B in the organism, increasing the halflife of the growth factor 50-fold . Latent TGF-f circulates in plasma at concentrations well above those necessary for TGF-f to elicit biological activity (Danielpour et al, 1989 (Knabbe et al, 1987;Glick et al, 1989;Oreffo et al, 1989;Colletta et al, 1990;Twardzik et al, 1990;Flaumenhaft et al, unpublished data). Activation of latent TGF-#1 also occurs in homotypic cultures of erythroleukemia cell lines (Piao et al, 1990) (Jullien et al, 1989;Pfeilschifter et al, 1990).…”

Section: Regulation In Time and Spacementioning

confidence: 99%

The extracellular regulation of growth factor action.

Flaumenhaft

Rifkin

1992

MBoC

163

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Section: Regulation In Time and Spacementioning

confidence: 99%

The extracellular regulation of growth factor action.

Flaumenhaft

Rifkin

1992

MBoC

163

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“…Transforming growth factor-␤ (TGF-␤) 1 is stored in bone matrix as a latent form (4), is thought to be released and activated during osteoclastic bone resorption (5), and to play an important role in the regulation of bone metabolism (6). TGF-␤ is one of the most potent stimulators of the production of type I collagen in various types of cells (7,8), and the most pronounced effect of TGF-␤ in bone is the stimulation of matrix protein synthesis including type I collagen, proteoglycans, and fibronectin (9,10).…”

mentioning

confidence: 99%

Differentiation and Cell Surface Expression of Transforming Growth Factor-β Receptors Are Regulated by Interaction with Matrix Collagen in Murine Osteoblastic Cells

Takeuchi

Nakayama

Matsumoto

1996

Journal of Biological Chemistry

194

142

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Although transforming growth factor (TGF)-␤ enhances bone formation, it inhibits the differentiation of osteoblasts. To clarify the regulatory mechanism of osteoblastic differentiation and TGF-␤ actions, the relationship among differentiation, TGF-␤ actions, and matrix protein synthesis was examined using murine osteoblast-like MC3T3-E1 cells. Alkaline phosphatase (ALP) activity continued to increase during long-term cultures, and the increase was closely associated with a reduction in cell surface TGF-␤ receptors competent to bind TGF-␤. Both the stimulation of proteoglycan synthesis and the inhibition of ALP activity by TGF-␤ were also suppressed. Collagen synthesis inhibitors and an anti-␣2␤1 integrin blocking antibody blocked the changes in ALP activity and TGF-␤ receptors, and a DGEA peptide that interferes binding of collagen to ␣2␤1 integrin also blocked the increase in ALP activity. Furthermore, when MC3T3-E1 cells were cultured on extracellular matrix layers obtained from these cells, all the differentiation-associated changes could be observed without collagen production, and the extracellular matrix-induced differentiation was also blocked by an anti-␣2␤1 integrin antibody. These results demonstrate that the interaction of cell surface ␣2␤1 integrin with matrix collagen synthesized by osteoblasts themselves is involved in the osteoblastic differentiation and the reduction in cell surface receptors and actions of TGF-␤. It is suggested that matrix collagen synthesized under the stimulation by TGF-␤ plays an important role in the regulation of osteoblastic differentiation and TGF-␤ actions by differentiation-associated down-regulation of TGF-␤ receptors.Cells of osteoblast lineage exert various functions to maintain bone formation. After bone resorption, osteoblast precursors migrate and proliferate at the site of bone formation. They, then, synthesize type I collagen and other matrix proteins. Onto the newly formed unmineralized matrices, hydroxyapatite crystals are accumulated, and mineralization of bone is completed (1). In order to form lamellar bones that maintain structural integrity and physical strength, it appears to be of critical importance for osteoblastic cells to maintain sequentially ordered development of these multiple functions.Using cultured osteoblastic cells obtained from bone or of clonal origin, it has become clear that these cells express various functional properties in a differentiation-dependent manner from the early proliferation phase, via the matrix formation phase with active matrix protein synthesis, to the mineralization phase (1-3). Various hormones and cytokines are shown to affect the differentiation process and functional properties of these cells. However, the mechanism that controls the differentiation of osteoblastic cells is as yet unclear.Transforming growth factor-␤ (TGF-␤) 1 is stored in bone matrix as a latent form (4), is thought to be released and activated during osteoclastic bone resorption (5), and to play an important role in the regulation of bone meta...

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“…Together with the protease study, cellular component of the TGF-P activation has been studied in various systems. As results, macrophage (Twardzik et al, 1990;Chong et al, 1999), mesenchymal cell (Rowley, 1992), cocultured endothelial cell with smooth muscle (Sato and Rifkin, 1989), and osteoclast (Oreffo et al, 1989) have been shown to be responsible for the cellular activation of latent TGF-P. Those cells may activate latent TGF-Ps through secreting or exposing protease on their cell surface. Recent knockout mice studies suggested thrombospondin-1 to be the enzyme responsible for the activation in vivo.…”

mentioning

confidence: 86%

Expression and activation of transforming growth factor‐beta 2 in cultured bone cells

Lee

2000

Korean Journal of Biological Sciences

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Activation of the bone-derived latent TGF beta complex by isolated osteoclasts

Cited by 272 publications

References 13 publications

The extracellular regulation of growth factor action.

The extracellular regulation of growth factor action.

Differentiation and Cell Surface Expression of Transforming Growth Factor-β Receptors Are Regulated by Interaction with Matrix Collagen in Murine Osteoblastic Cells

Expression and activation of transforming growth factor‐beta 2 in cultured bone cells

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