Different activation of mitogen-activated protein kinases in experimental proliferative glomerulonephritis. Kidney Int Suppl 1998 Sep;67:S189-91
Date
09/15/1998Pubmed ID
9736286DOI
10.1046/j.1523-1755.1998.06743.xScopus ID
2-s2.0-0031721659 (requires institutional sign-in at Scopus site) 12 CitationsAbstract
Mitogen-activated protein (MAP) kinases are critical for cell signaling goals such as cellular proliferation and induction of apoptosis. We examined whether MAP kinases, as a point of convergence for multiple extracellular stimuli, are activated in proliferative glomerulonephritis (GN) in vivo. Accelerated crescentic anti-glomerular basement membrane (GBM) GN was induced in rats preimmunized with rabbit IgG by administration of rabbit anti-rat GBM serum. Whole cortical tissue and isolated glomeruli were then subjected to kinase activity assays and Western blot analysis. Cortical activity of the archetypal MAP kinase, extracellular signal-regulated kinase (ERK), was increased significantly one, three, and seven days after induction of GN. In contrast, activation of MAP kinases with antiproliferative actions, stress-activated protein kinase, and p38 MAP kinase was detectable only in the early stages of proliferative GN (days one and three), implying that different MAP kinases serve distinct roles in the pathogenesis of GN.
Author List
Bokemeyer D, Guglielmi KE, McGinty A, Sorokin A, Lianos EA, Dunn MJAuthor
Andrey Sorokin PhD Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsBlotting, Western
Calcium-Calmodulin-Dependent Protein Kinases
Enzyme Activation
Glomerulonephritis, Membranoproliferative
Kidney Glomerulus
Male
Mitogen-Activated Protein Kinase 3
Mitogen-Activated Protein Kinases
Rabbits
Rats
Rats, Sprague-Dawley
p38 Mitogen-Activated Protein Kinases
