The effects of exogenous growth factors on matrix metalloproteinase secretion by human brain tumour cells

Rooprai, Harcharan K.; Rucklidge, Garry J.; Panou, Charalampos; Pilkington, Geoffrey J.

doi:10.1054/bjoc.1999.0876

Cited by 98 publications

(60 citation statements)

References 24 publications

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“…Similar to Nodal, MMP-2 has also been implicated in embryogenesis and tumor invasion (Rooprai et al, 2000). In this study, we showed that the ectopic expression of Nodal or activation of Nodal signaling by addition of rNodal increased MMP-2 protein level and cell invasion.…”

Section: Discussionsupporting

confidence: 54%

Nodal promotes growth and invasion in human gliomas

et al. 2010

Oncogene

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Section: Discussionsupporting

confidence: 54%

Nodal promotes growth and invasion in human gliomas

et al. 2010

Oncogene

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“…Regarding the angiogenic effects of VEGF and Ang-1, several studies have evaluated the role of these molecules in the regulation of gelatinases during angiogenesis. In vitro, VEGF increases both expression and release of MMP-2 and MMP-9 (Lamoreaux et al, 1998;Rooprai et al, 2000;Wang and Keiser, 1998). More recently, Ang-1 have been also described to interfere with MMP-2 and MMP-9 expressions (Das et al, 2003;Kim et al, 2000).…”

Section: Discussionmentioning

confidence: 97%

VEGF-Induced BBB Permeability is Associated with an MMP-9 Activity Increase in Cerebral ischemia: Both Effects Decreased by ANG-1

Valable

Montaner

Bellail

et al. 2005

J Cereb Blood Flow Metab

177

125

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After cerebral ischemia, angiogenesis, by supplying for the deficient perfusion, may be a beneficial process for limiting neuronal death and promoting tissue repair. In this study, we showed that the combination of Ang-1 and vascular endothelial growth factor (VEGF) provides a more adapted therapeutic strategy than the use of VEGF alone. Indeed, we showed on a focal ischemia model that an early administration of VEGF exacerbates ischemic damage, because of its effects on bloodbrain barrier (BBB) permeability. In contrast, a coapplication of Ang-1 and VEGF leads to a significant reduction of the ischemic and edema volumes by 50% and 42%, respectively, in comparison with VEGF-treated mice. We proposed that Ang-1 blocks the BBB permeability effect of VEGF in association with a modulation of matrix metalloproteinase (MMP) activity. Indeed, we showed on both ischemic in vivo and BBB in vitro models that VEGF enhances BBB damage and MMP-9 activity and that Ang-1 counteracts both effects. However, we also showed a synergic angiogenic effect of Ang-1 and VEGF in the brain. Taken together, these results allow to propose that, in cerebral ischemia, the combination of Ang-1 and VEGF could be used early to promote the formation of mature neovessels without inducing side effects on BBB permeability.

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“…In the literature, there are only a few reports of MMP-9 upregulation by this growth factor in human aortic smooth muscle cells (75), human brain tumor cells (76), and human myelo-monocytic leukemia cell lines (74). However, there are no reports demonstrating the up-regulation of MMP-9 in T cells by this growth factor.…”

Section: Discussionmentioning

confidence: 99%

Up-Regulation of Matrix Metalloproteinase-9 in T Lymphocytes of Mammary Tumor Bearers: Role of Vascular Endothelial Growth Factor

Owen

Iragavarapu-Charyulu

Gunja‐Smith

et al. 2003

The Journal of Immunology

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Matrix metalloproteinase-9 (MMP-9), a matrix-degrading enzyme, is crucial in tumor invasion and metastasis and is implicated in leukocyte extravasation. In this report, we demonstrate that during growth of the D1–7,12-dimethylbenzanthracene-3 mammary tumor in BALB/c mice, there is progressive up-regulation of MMP-9 in splenic T cells at both the transcriptional and translational levels. Our previous work has identified several factors produced by this tumor, including PGE2, GM-CSF, and phosphatidyl serine; however, none of these agents induces increased production of MMP-9 by normal splenic T cells. Although not produced by the tumor, TNF-α and IL-6 are up-regulated in both macrophages and B cells in tumor-bearing mice. Exposure of normal T cells to these two cytokines, however, also fails to up-regulate MMP-9 production. Vascular endothelial growth factor (VEGF) is produced by many tumors, and we determined that the mammary tumor used in our studies expresses high levels of this angiogenic growth factor. Importantly, splenic T cells from tumor bearers constitutively produce increased amounts of VEGF, and treatment of normal T cells with VEGF results in up-regulated MMP-9 production. Of crucial importance is the finding that tumor-infiltrating T cells also produce high levels of VEGF and MMP-9. Our studies indicate that VEGF can act directly on T lymphocytes and that elevated VEGF levels may contribute to the aberrant MMP-9 secretion by mammary tumor bearers’ T cells.

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The effects of exogenous growth factors on matrix metalloproteinase secretion by human brain tumour cells

Cited by 98 publications

References 24 publications

Nodal promotes growth and invasion in human gliomas

Nodal promotes growth and invasion in human gliomas

VEGF-Induced BBB Permeability is Associated with an MMP-9 Activity Increase in Cerebral ischemia: Both Effects Decreased by ANG-1

Up-Regulation of Matrix Metalloproteinase-9 in T Lymphocytes of Mammary Tumor Bearers: Role of Vascular Endothelial Growth Factor

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