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Endostatin expression in a pancreatic cell line is modulated by a TNFalpha-dependent elastase.

Brammer RD, Bramhall SR, Eggo MC - Br. J. Cancer (2005)

Bottom Line: Precursor forms only were found in the cells.Elastase activity was found in cell extracts but not the cell-conditioned media of SUIT-2 cells.We conclude that endostatin is released by SUIT-2 cells and that increases in intracellular elastase, induced by TNFalpha, are correlated with increased secretion.

View Article: PubMed Central - PubMed

Affiliation: Division of Medical Sciences, University of Birmingham, Birmingham B15 2TT, UK.

ABSTRACT
Endostatin, an inhibitor of angiogenesis, is a 20 kDa fragment of the basement membrane protein, collagen XVIII. The formation of endostatin relies upon the action of proteases on collagen XVIII. TNFalpha, produced by activated macrophages, is a multifunctional proinflammatory cytokine with known effects on endothelial function. We postulated that TNFalpha may modulate the activities of proteases and thus regulate endostatin formation in pancreatic cells. Collagen XVIII/endostatin mRNA was expressed in one pancreatic cell line, SUIT-2, but not in BxPc-3. The 20 kDa endostatin was found in the cell-conditioned medium of SUIT-2 cells. Precursor forms only were found in the cells. Exogenous endostatin was degraded by cellular lysates of SUIT-2 cells. Elastase activity was found in cell extracts but not the cell-conditioned media of SUIT-2 cells. Incubation of SUIT-2 cells with TNFalpha increased intracellular elastase activity and also increased secretion of endostatin into the medium. We conclude that endostatin is released by SUIT-2 cells and that increases in intracellular elastase, induced by TNFalpha, are correlated with increased secretion. Endostatin is however susceptible to degradation by intracellular proteases and if tissue injury accompanies inflammation, endostatin may be degraded, allowing angiogenesis to occur.

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Related in: MedlinePlus

Rate of hydrolysis of the elastase substrate by SUIT-2 cell extract and serum-free cell-conditioned culture media.
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fig4: Rate of hydrolysis of the elastase substrate by SUIT-2 cell extract and serum-free cell-conditioned culture media.

Mentions: Elastase activity, measured by the colorimetric method, in the cell extracts and in 48 h collection of serum-free cell conditioned medium is shown in Figure 4. There was detectable elastase in the cell layer yet there was none in the 48 h cell-conditioned medium.


Endostatin expression in a pancreatic cell line is modulated by a TNFalpha-dependent elastase.

Brammer RD, Bramhall SR, Eggo MC - Br. J. Cancer (2005)

Rate of hydrolysis of the elastase substrate by SUIT-2 cell extract and serum-free cell-conditioned culture media.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2361670&req=5

fig4: Rate of hydrolysis of the elastase substrate by SUIT-2 cell extract and serum-free cell-conditioned culture media.
Mentions: Elastase activity, measured by the colorimetric method, in the cell extracts and in 48 h collection of serum-free cell conditioned medium is shown in Figure 4. There was detectable elastase in the cell layer yet there was none in the 48 h cell-conditioned medium.

Bottom Line: Precursor forms only were found in the cells.Elastase activity was found in cell extracts but not the cell-conditioned media of SUIT-2 cells.We conclude that endostatin is released by SUIT-2 cells and that increases in intracellular elastase, induced by TNFalpha, are correlated with increased secretion.

View Article: PubMed Central - PubMed

Affiliation: Division of Medical Sciences, University of Birmingham, Birmingham B15 2TT, UK.

ABSTRACT
Endostatin, an inhibitor of angiogenesis, is a 20 kDa fragment of the basement membrane protein, collagen XVIII. The formation of endostatin relies upon the action of proteases on collagen XVIII. TNFalpha, produced by activated macrophages, is a multifunctional proinflammatory cytokine with known effects on endothelial function. We postulated that TNFalpha may modulate the activities of proteases and thus regulate endostatin formation in pancreatic cells. Collagen XVIII/endostatin mRNA was expressed in one pancreatic cell line, SUIT-2, but not in BxPc-3. The 20 kDa endostatin was found in the cell-conditioned medium of SUIT-2 cells. Precursor forms only were found in the cells. Exogenous endostatin was degraded by cellular lysates of SUIT-2 cells. Elastase activity was found in cell extracts but not the cell-conditioned media of SUIT-2 cells. Incubation of SUIT-2 cells with TNFalpha increased intracellular elastase activity and also increased secretion of endostatin into the medium. We conclude that endostatin is released by SUIT-2 cells and that increases in intracellular elastase, induced by TNFalpha, are correlated with increased secretion. Endostatin is however susceptible to degradation by intracellular proteases and if tissue injury accompanies inflammation, endostatin may be degraded, allowing angiogenesis to occur.

Show MeSH
Related in: MedlinePlus