Expression of Ser729 phosphorylated PKCepsilon in experimental crescentic glomerulonephritis: an immunohistochemical study

• Published in: European journal of histochemistry 2014-04, Vol.58 (2), p.2308-2308
• Main Authors: Karavana, V N, Gakiopoulou, H, Lianos, E A
• Format: Article
• Language: English
• Subjects: Animals; Antimetabolites, Antineoplastic - adverse effects; Antimetabolites, Antineoplastic - pharmacology; crescents; Epithelial Cells - enzymology; Epithelial Cells - pathology; Gene Expression Regulation, Enzymologic; Glomerulonephritis; Glomerulonephritis - chemically induced; Glomerulonephritis - enzymology; Glomerulonephritis - pathology; Kidney Glomerulus - enzymology; Kidney Glomerulus - pathology; Myofibroblasts - enzymology; Myofibroblasts - pathology; phosphorylation; Phosphorylation - drug effects; PKCepsilon; podocytes; Protein Kinase C-epsilon - biosynthesis; Puromycin - adverse effects; Puromycin - pharmacology; Rats; Rats, Sprague-Dawley; Serine - metabolism
• ISSN: 1121-760X; 2038-8306
• DOI: 10.4081/ejh.2014.2308

PKCε, a DAG-dependent, Ca2+- independent kinase attenuates extent of fibrosis following tissue injury, suppresses apoptosis and promotes cell quiescence. In crescentic glomerulonephritis (CGN), glomerular epithelial cells (GEC) contribute to fibro-cellular crescent formation while they also transdifferentiate to a mesenchymal phenotype. The aim of this study was to assess PKCε expression in CGN. Using an antibody against PKC-ε phosphorylated at Ser729, we assessed its localization in rat model of immune-mediated rapidly progressive CGN. In glomeruli of control animals, pPKCε was undetectable. In animals with CGN, pPKCε was expressed exclusively in glomerular epithelial cells (GEC) and in GEC comprising fibrocellular crescents that had acquired a myofibroblast-type phenotype. In non-immune GEC injury induced by puromycin aminonucleoside and resulting in proteinuria of similar magnitude as in CGN, pPKCε expression was absent. There was constitutive pPKCε expression in distal convoluted tubules, collecting ducts and thick segments of Henley's loops in both control and experimental animals. We propose that pPKCε expression occurring in GEC and in fibrocellular crescentic lesions in CGN may facilitate PKCε dependent pathologic processes.