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Annals of Clinical & Laboratory Science 40:26-31 (2010)
© 2010 Association of Clinical Scientists

Fluprostenol-Induced MAPK Signaling Is Independent of Aging in Fischer 344/NNiaHSd x Brown Norway/BiNia Rat Aorta

Kevin M. Rice1,2,3,4, Ernest M. Walker5, Sunil K Kakarla3,4,6, Satyanarayana Paturi1,3,4, Miaozong Wu1,3, Sumit Narula4 and Eric R. Blough1,2,3,4,6
1 Department of Biological Sciences, 2 Department of Exercise Science, Sport and Recreation, 3 Cell Differentiation and Development Center, 4 Laboratory of Molecular Physiology, 5 Department of Anatomy and Pathology, and 6 Department of Pharmacology, Physiology, and Toxicology, Marshall University, Huntington, West Virginia

Address correspondence to Eric Blough, Ph.D., Room 241N, Robert C. Byrd Biotechnology Science Center, Marshall University, 1700 3rd Ave., Huntington, WV 25755-1090, USA; tel 304 696 2708; e-mail: blough{at}marshall.edu.

The factors that regulate vascular mechanotransduction and how this process may be altered with aging are poorly understood and have not been widely studied. Recent data suggest that increased tissue loading can result in the release of prostaglandin F2 alpha (PGF2{alpha}) and other reports indicate that aging diminishes the ability of the aged aorta to activate mitogen activated protein kinase (MAPK) signaling in response to increased loading. Using ex vivo incubations, here we investigate whether aging affects the ability of the aorta to induce phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2-MAPK), p38-MAPK, and Jun N-terminal kinase (JNK-MAPK) activation following stimulation with a PGF2{alpha} analog, fluprostenol. Compared to aortas from 6-mo animals, the amounts of ERK1/2- and p38-MAPK remained unchanged with aging, while the level of JNK-MAPK protein increased by 135% and 100% at 30- and 36-mo, respectively. Aging increased the basal phosphorylation of ERK1/2 (115% and 47%) and JNK (29% and 69%) (p <0.05) in 30- and 36-mo aortas, while p38 phosphorylation levels remained unaltered. Compared to age-matched controls, fluprostenol induced phosphorylation of ERK1/2 (310%, 286%, and 554%), p38-MAPK (unchanged, 48%, and 148%), and JNK (78%, 88%, and 95%) in 6-, 30- and 36-mo aortas, respectively. These findings suggest that aging does not affect the ability of the rat aorta to activate ERK1/2-, p38-MAPK, and JNK-MAPK phosphorylation in response to PGF2{alpha} stimulation.

Keywords: aorta, fluprostenol, ERK1/2, p38-MAPK, JNK, aging






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