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Experimental Physiology 92.5 pp 963-970
DOI: 10.1113/expphysiol.2007.037275
© The Physiological Society 2007
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Uniaxial stretch-induced regulation of mitogen-activated protein kinase, Akt and p70 S6 kinase in the ageing Fischer 344 x Brown Norway rat aorta

 Kevin M. Rice1,2, Devashish H. Desai2, Deborah L. Preston1, Paulette S. Wehner3 and Eric R. Blough1,2

1 Department of Biological Sciences, Marshall University, Huntington, WV, USA Departments of 2 Pharmacology, Physiology and Toxicology3 Cardiology, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV, USA

The effects of ageing on the cardiovascular system contribute to substantial alterations in cellular morphology and function. The variables regulating these changes are unknown; however, one set of signalling molecules that may be of particular importance in mediating numerous cellular responses, including control of cell growth, differentiation and adaptation, are the proteins associated with the mitogen-activated protein kinase (MAPK) signalling systems. The MAPKs, in conjunction with the p70 S6k signalling cascade, have emerged as critical components for regulating numerous mechanotransduction-related cellular responses. Here we investigate the ability of uniaxial stretch to activate the MAPK and p70 S6k pathways in adult (6-month-old), aged (30-month-old) and very aged (36-month-old) Fischer 344/NNiaHSd x Brown Norway/BiNia (FBN) rats. Western blotting of the MAPK family proteins extracellular signal-regulated kinase (Erk) 1/2, p38- and c-Jun NH2-terminal kinase (Jnk)-MAPKs showed differential expression and activation between these proteins with age. An acute 15 min interval of 20% uniaxial stretch using an ex vivo aortic preparation demonstrated similar regulation of Erk1/2, p38- and Jnk-MAPK. However, ageing altered uniaxial induced p70 S6k pathway signalling. These observations confirm previous data demonstrating that MAPK proteins are mechanically regulated and also suggest that p70 S6k signalling expression and activation are controlled differently with ageing. Taken together, these data may help to explain, in part, the age-related changes in vascular morphology, function and response to injury.

(Received 9 February 2007; accepted after revision 24 May 2007; first published online 25 May 2007)
Corresponding author E. Blough: Laboratory of Molecular Physiology, Suite 311, Science Building, Department of Biological Sciences, 1 John Marshall Drive, Marshall University, Huntington, WV 25755-1090, USA. Email: blough{at}marshall.edu






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Copyright © 2007 by the The Physiological Society.