PMID: 8587480Jan 1, 1995Paper

ET-1 and PDGF BB induce MEK mRNA and protein expression in mesangial cells

Journal of Cardiovascular Pharmacology
H SchramekM J Dunn

Abstract

To evaluate a possible mechanism for the chronic regulation of MAPK/ERK kinase-1 (MEK-1) and p42 mitogen-activated protein kinase (MAPK) we studied the long-term effects of the G-protein-coupled receptor agonist endothelin-1 (ET-1) and the protein tyrosine kinase-coupled receptor agonist platelet-derived growth factor BB (PDGF BB) on MEK-1 and p42 MAPK in glomerular mesangial cells (GMCs). ET-1 and PDGF BB led to a time-dependent increase in MEK-1 mRNA expression without altering p42 MAPK mRNA levels. The effect of ET-1 and PDGF BB on MEK-1 mRNA expression was maximal after 24 h (3.3-fold) or 6 h (2.9-fold). Furthermore, the effect of ET-1 and PDGF BB on MEK-1 mRNA expression was additive (4.2-fold after 6 h) and was inhibited by actinomycin D (5 micrograms/ml). Cycloheximide (10 micrograms/ml) inhibited MEK-1 mRNA induction but stimulated p42 MAPK mRNA expression in both the absence and the presence of ET-1 and/or PDGF BB. The ET-1 and PDGF BB-induced increase in MEK-1 mRNA was accompanied by sustained enhancement of both p45 MEK protein expression after 12 h and by elevation of p42 MAPK activity for up to 24 h. We conclude that, in GMCs, MEK-1 acts like a delayed-early gene, whereas p42 MAPK resembles an immediate-early gene....Continue Reading

Citations

Feb 13, 1999·Kidney International·A J IngramJ W Scholey
May 1, 1996·Kidney International·D BokemeyerM J Dunn
May 26, 2005·Brain Research. Brain Research Reviews·Lyle W Ostrow, Frederick Sachs
Apr 25, 2012·Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association·Younghyun LeeHai Won Chung

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