Skip to main content
Log in

Induction of macrophage plasminogen activator by asbestos is independent of PKC activation

  • Original Investigations
  • Published:
Archives of Toxicology Aims and scope Submit manuscript

Abstract

This study was undertaken to assess whether plasminogen activator (PA) induction in macrophages exposed to chrysotile fibers is mediated by protein kinase C (PKC) activation. In PKC depleted J774 cells, PA induction could be elicited by chrysotile whereas, as expected, the response to phorbol myristate acetate (PMA) was abolished. The effect of PMA and chrysotile on the distribution of PKC activity in the J774 cell line was also compared by measuring the enzyme catalytic activity and phorbol dibutyrate (PDBu) binding sites. No redistribution of PKC was observed after stimulation with PA inducing doses of chrysotile, whereas a clear translocation was observed with PMA. It is concluded that the mechanism of PA induction by chrysotile in this macrophage-like cell line is independent of PKC activation.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

References

  • Cantin A, Allard C, Begin R (1989) Increased alveolar plasminogen activator in early asbestosis. Am Rev Resp Dis 139: 604–609

    Google Scholar 

  • Crooke ST, Snyder RM, Butt TR, Ecker DJ, Allaudeen, Monia B, Mirabelli CK (1986) Cellular and molecular pharmacology of auranofin and related gold complex. Biochem Pharmacol 35: 3423–3431

    Google Scholar 

  • Hamilton J, Vassalli J-D, Reich E (1976) Macrophage plasminogen activator: induction by asbestos is blocked by anti-inflammatory steroids. J Exp Med 144: 1689–1694

    Google Scholar 

  • Knoops B, Lison D, Collette C, Lauwerys R, Picard J-J (1989) Plasminogen activator activity of normal and retinoic acid-treated post-implantation embryos. Biochem Pharmacol 39: 1545–1548

    Google Scholar 

  • Lison D, Knoops B, Lauwerys R (1989) Effect of retinoic acid on asbestos-induced plasminogen activator activity of peritoneal macrophages. Br J Ind Med 46: 496–497

    Google Scholar 

  • Lison D, Raguzzi F, Lauwerys R (1990) Comparison of the effects of auranofin, heavy metals and retinoids on protein kinase C in vitro and on a protein kinase C mediated response in macrophages. Pharmacol Toxicol 67: 239–242

    Google Scholar 

  • Mossmann BT, Light W, Wei E (1983) Asbestos: mechanism of toxicity and carcinogenicity in the respiratory tract. Annu Rev Pharmacol Toxicol 23: 595–615

    Google Scholar 

  • Nishizuka Y (1988) The molecular heterogeneity of protein kinase C and its implications for cellular regulation. Nature 334: 661–665

    Google Scholar 

  • Robinson BWS (1988) Production of plasminogen activator by alveolar macrophages in normal subjects and in patients with interstitial lung disease. Thorax 43: 508–515

    Google Scholar 

  • Roney PL, Holian A (1989) Possible mechanism of chrysotile asbestos-stimulated Superoxide anion production in guinea pig alveolar macrophages. Toxicol Appl Pharmacol 100: 132–144

    Google Scholar 

  • Wallenstein S, Zucker CL, Fleiss JL (1980) Some statistical methods useful in circulation research. Circ Res 47: 1–9

    Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

About this article

Cite this article

Lison, D., Raguzzi, F. & Lauwerys, R. Induction of macrophage plasminogen activator by asbestos is independent of PKC activation. Arch Toxicol 65, 386–389 (1991). https://doi.org/10.1007/BF02284261

Download citation

  • Received:

  • Revised:

  • Accepted:

  • Issue Date:

  • DOI: https://doi.org/10.1007/BF02284261

Key words

Navigation