Modulation by Soluble Factors of Gelatinase Activities Released by Osteoblastic Cells

Damiens, Christelle; Fortun, Yannick; Charrier, Céline; Heymann, Dominique; Pocard, Marc

doi:10.1006/cyto.2000.0765

Cited by 23 publications

(12 citation statements)

References 16 publications

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“…This deletion, between the membrane spanning and death domain motifs, is out of frame and changes GCA GAT, Ala‐Asp, to G‐AT, Asp with the loss of an alanine. This deletion is at a position where alanine occurs once (GenBank U94501) or twice (U94502) in previously reported DR3 transcripts (Warzocha et al, 1998; Damiens et al, 2000). Because some putative DR3 ligands activate FN14, we studied the expression of this alternate TNF receptor by PCR.…”

Section: Resultsmentioning

confidence: 93%

“…Another circumstance that may promote membrane signaling is where transmembrane signaling DR3 is highly expressed. Overexpression of DR3 in 293‐T human embryonic kidney or 3T3 fibroblast cells causes caspase 8‐dependent apoptosis as well as activation of NF‐κB (Bodmer et al, 1997; Damiens et al, 2000), while apoptosis in TF1 cells by anti‐DR3 requires cycloheximide sensitization (Wen et al, 2003), but DR3 activation using TL1A in phytohemagglutin‐activated T cells does not promote apoptosis but supports proliferation (Migone et al, 2002). Our flow data show that DR3 expression does vary in subgroups of MG63 cells, but we do not know of specific circumstances that promote DR3 expression.…”

Section: Discussionmentioning

confidence: 99%

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Death receptor‐3 mediates apoptosis in human osteoblasts under narrowly regulated conditions

Borysenko

García-Palacios

Griswold

et al. 2006

Journal Cellular Physiology

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We previously reported that a soluble form of the TNF-family receptor death receptor-3 (DR3) is expressed in osteoblasts. DR3 regulates death or differentiation in other tissues, and DR3 ligands occur in bone, but the function of DR3 in the osteoblast was unknown. We studied the expression of DR3 and the effects crosslinking antibodies to DR3 or of natural DR3 ligands in human osteoblasts. Western analysis showed that nontransformed osteoblasts and the MG63 osteosarcoma cell line produce both soluble decoy receptor and transmembrane isoforms of DR3. Cell surface labeling showed that low and high DR3-expressing osteoblast populations occur. Verification of by cloning showed a point mutation in DR3 from MG63 cells. Activation of DR3 by antibody crosslinking or with DR3 ligands caused apoptosis in osteoblasts and in MG63 cells, but only in low-density cell cultures. In dense cultures apoptosis did not occur, but nuclear factor-kappaB nuclear translocation was observed under some conditions. Crosslinking of DR3 in high-density MG63 cultures blocked expression of bone matrix elements. DR3 activation in high-density nontransformed osteoblasts had only minor effects on cell maturation. We conclude that DR3 activation can mediate apoptosis in osteoblasts. Its activity is, however, highly restricted by its soluble ligand-binding isoform and possibly also by alternate survival signals. In the presence of survival signals, DR3 may affect cell maturation although effects on differentiation were clearly seen only in the MG63 transformed cell line.

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Section: Resultsmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Death receptor‐3 mediates apoptosis in human osteoblasts under narrowly regulated conditions

Borysenko

García-Palacios

Griswold

et al. 2006

Journal Cellular Physiology

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“…Then the TNF-αinduced production of IL-6 in osteoblasts was examined and it was found that, in accord with a previous report (Choi and Koo, 2002), TNF-α upregulated IL-6 production in osteoblasts. IL-6 induces osteoblasts to resorb bone (Kotake et al, 1996) and stimulates osteoblasts to produce matrix metalloproteinases (MMPs, Damiens et al, 2000). As IL-6 stimulates the production of MMPs by osteoblasts (Damiens et al, 2000), it could be possible that in our experiments TNFα stimulated the osteoblasts to release IL-6 and that IL-6 in turn stimulated these cells to release pro-MMPs.…”

Section: Effect Of Cce On Osteoblastic Mc3t3-e1 Cell Apoptosismentioning

confidence: 80%

Stimulatory effects of extract prepared from the bark of Cinnamomum cassia blume on the function of osteoblastic MC3T3‐E1 cells

Lee

Choi

2006

Phytotherapy Research

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The ethanol extract from the bark of Cinnamomum cassia Blume (CCE) was tested for estrogenic activity. CCE (4-60 microg/mL) significantly induced the growth of MCF-7 cells, an ER-positive human breast cancer cell line, over that of untreated control cells (p < 0.05). In the ER competitive binding assay, CCE showed higher affinity with ERbeta compared with ERalpha. To investigate the bioactivities of CCE, which act on bone metabolism, the effects of CCE on the function of osteoblastic MC3T3-E1 cells and the production of local factors in osteoblasts were studied. CCE (4-60 microg/mL) dose-dependently increased the survival of MC3T3-E1 cells. In addition, CCE (10 and 50 microg/mL) increased alkaline phosphatase (ALP) activity, collagen synthesis and osteocalcin secretion in MC3T3-E1 cells. Treatment with CCE (10 and 50 microg/mL) prevented apoptosis induced by TNF-alpha (10(-10) m) in osteoblastic cells. In the presence of TNF-alpha, culture with CCE (10-100 microg/mL) for 48 h inhibited the production of IL-6 and nitric oxide in osteoblastic MC3T3-E1 cells. These results suggest that Cinnamomum cassia has a direct stimulatory effect on bone formation in vitro and may contribute to the prevention of osteoporosis and inflammatory bone diseases.

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“…OSM increased MMP-2 expression in rat aortic smooth muscle cells (SMC) (Nagata et al, 2003). In contrast, there was no modulation of MMP-2 expression/activity in the presence of OSM in normal human osteoblasts or osteogenic sarcoma cells (Damiens et al, 2000). Regarding MMP-9, it has been shown that OSM enhances MMP-9 expression in fibroblasts (Korzus et al, 1997) and SMC (Nagata et al, 2003), but failed to affect the expression of MMP-9 in osteoblasts (Varghese et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Divergent effects of oncostatin M on astroglioma cells: Influence on cell proliferation, invasion, and expression of matrix metalloproteinases

Chen

Gillespie

Benveniste

2005

Glia

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Oncostatin M (OSM), a cytokine of the interleukin-6 (IL-6) family, can either promote or inhibit cell growth in various normal and tumor cells. We addressed the effects of exogenous OSM on the proliferation and invasion of human astroglioma cells. In addition, we investigated one of the possible mechanisms involved: modulation of matrix metalloproteinase (MMP) expression and enzymatic activity. We found that OSM inhibited the proliferation of two human astroglioma cell lines (CH235-MG and U87-MG), and that this effect was not due to apoptosis. The inhibitory effect of OSM on proliferation was mediated through the gp130/OSMRbeta receptor complex. To extend these findings, we analyzed the effects of OSM on primary tumor cells from glioblastoma patients. OSM suppressed the proliferation of primary glioblastoma cells, but not that of normal astrocytes. Interestingly, OSM did not suppress astroglioma cell invasion. This may be due to the differential regulation of MMPs by OSM. We found that OSM inhibited the constitutive expression of MMP-2, while MMP-9 expression was enhanced in astroglioma cell lines. We conclude that OSM inhibits proliferation of human astroglioma cells and primary glioblastoma cells via the gp130/OSMRbeta receptor complex. However, OSM does not affect the invasive capacity of the astroglioma cells, which may be due to the divergent effects of OSM on MMP-2 and MMP-9 expression. Collectively, these findings suggest a complex role for OSM in astroglioma biology.

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Modulation by Soluble Factors of Gelatinase Activities Released by Osteoblastic Cells

Cited by 23 publications

References 16 publications

Death receptor‐3 mediates apoptosis in human osteoblasts under narrowly regulated conditions

Death receptor‐3 mediates apoptosis in human osteoblasts under narrowly regulated conditions

Stimulatory effects of extract prepared from the bark of Cinnamomum cassia blume on the function of osteoblastic MC3T3‐E1 cells

Divergent effects of oncostatin M on astroglioma cells: Influence on cell proliferation, invasion, and expression of matrix metalloproteinases

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