Mr. Nicholas Von Offenberg Sweeney VHRC Logo

NICHOLAS VON OFFENBERG SWEENEY, B.Sc.

Postgraduate Research Student

  • 2000-date: Postgraduate Student, School of Biotechnology, Dublin City University.
  • 1996-2000: B.Sc. in Biotechnology, School of Biotechnology, Dublin City University.
  • 1999: Research Assistant, L'Ecole Desmines, D'Ales, France.

Ongoing Research

  • Mechanical force regulation of matrix metalloproteinases (MMPs) in vascular endothelial and smooth muscle cells

    Matrix metalloproteinases are a diverse family of enzymes which play a major role in angiogenesis and cellular migration. In certain disease states such as arteriosclerosis, the hemodynamic forces to which cells are exposed change dramatically. Using novel perfused transcapillary co-culture and Flexercell® Tension Plus™ FX-4000T™ systems to expose vascular cells to physiological levels of shear stress and cyclic strain, respectively, we can examine how mechanical forces affect the regulation of MMP expression and activity in vitro. Our main interests include (i) the effect of mechanical forces on MMP levels, (ii) how is this effect mediated (Integrins, G-proteins, ion channels etc.) and (iii) the subsequent effect on cell migration.

Recent Publications

  • Guibal, E., Von Offenberg Sweeney, N., Zikan, M.C., Vincent, T. and Tobin, J.M. (2001). Competitive sorption of platinum and palladium on chitosan derivatives. Int J Biol Macromol 12: 401-8.
  • Guibal, E., Von Offenberg Sweeney, N., Vincent, T. and Tobin, J.M. (2001). Title... React Funct Polym, submitted.

Recent Abstracts/Posters

  • Von Offenberg Sweeney, N., Birney, Y., Cummins, P.M. and Cahill, P.A. (2002). Cyclic strain Induces pro-MMP2 release from bovine aortic endothelial cells via a Gia protein-independent pathway and via a MAP kinase-dependent pathway. ExBio 2002 FASEB Meeting: 'Translating the Genome', New Orleans, LA.
  • Von Offenberg Sweeney, N., Coen, P., Cummins, P. and Cahill, P.A. (2001). Shear stress induced pro-MMP2 activity in bovine aortic endothelial cells via an inhibitory Gi protein. Ir J Med Sci 170 (suppl 2): 124.

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