Picture of aircraft jet engine

Strathclyde research that powers aerospace engineering...

The Strathprints institutional repository is a digital archive of University of Strathclyde's Open Access research outputs. Strathprints provides access to thousands of Open Access research papers by University of Strathclyde researchers, including by Strathclyde researchers involved in aerospace engineering and from the Advanced Space Concepts Laboratory - but also other internationally significant research from within the Department of Mechanical & Aerospace Engineering. Discover why Strathclyde is powering international aerospace research...

Strathprints also exposes world leading research from the Faculties of Science, Engineering, Humanities & Social Sciences, and from the Strathclyde Business School.

Discover more...

Inhibition of cell growth by lovastatin

Winn, P.L. and Kelso, K. and Grant, M.H. (2004) Inhibition of cell growth by lovastatin. Toxicology, 202 (1-2). pp. 106-107. ISSN 0300-483X

Full text not available in this repository. (Request a copy from the Strathclyde author)

Abstract

Lovastatin has been shown to be a potent inhibitor of smooth muscle cell (SMC) growth (Liao et al., 2002; Mattingly et al., 2002). The drug is a competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By inhibiting mevalonate (MVA) synthesis, lovastatin prevents the synthesis of isoprenoid intermediates which serve as lipid attachments for post-translational modification of various cell signalling proteins (Munro et al., 1994). Ras and Rho B proteins are major substrates for post-translational modification by isoprenylation. Since they regulate cell growth, studies have suggested lovastatin inhibits DNA synthesis and SMC growth by inhibiting isoprenylation of key signalling proteins (Raiteri et al., 1997). The aim of our study was to find out if the inhibition of SMC growth by lovastatin is caused by inhibition of HMG-CoA and could therefore be reversed by MVA.