@article{3159957,
    title = "Expression of Ser(729) phosphorylated PKCepsilon in experimental
crescentic glomerulonephritis: an immunohistochemical study",
    author = "Karavana, V. N. and Gakiopoulou, H. and Lianos, E. A.",
    journal = "European Journal of Histochemistry",
    year = "2014",
    volume = "58",
    number = "2",
    pages = "88-94",
    publisher = "PAGEPRESS PUBL",
    issn = "1121-760X",
    doi = "10.4081/ejh.2014.2308",
    keywords = "glomerulonephritis; crescents; PKCepsilon; podocytes; phosphorylation",
    abstract = "PKCe, 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 PKCe expression in CGN. Using an antibody
against PKC-epsilon phosphorylated at Ser(729), we assessed its
localization in rat model of immune-mediated rapidly progressive CGN. In
glomeruli of control animals, pPKC epsilon was undetectable. In animals
with CGN, pPKC epsilon was expressed exclusively in glomerular
epithelial cells (GEC) and in GEC comprising fibrocellular crescents
that had acquired a myofibroblasttype phenotype. In non-immune GEC
injury induced by puromycin aminonucleoside and resulting in proteinuria
of similar magnitude as in CGN, pPKCe expression was absent. There was
constitutive pPKC epsilon expression in distal convoluted tubules,
collecting ducts and thick segments of Henley’s loops in both control
and experimental animals. We propose that pPKCe expression occurring in
GEC and in fibrocellular crescentic lesions in CGN may facilitate PKCe
dependent pathologic processes."
}