title: De novo expression of podocyte proteins in parietal epithelial cells during experimental glomerular disease.
abstract: Studies have shown that certain cells of the glomerular tuft begin to express proteins considered unique to other cell types upon injury. Little is known about the response of parietal epithelial cells (PEC) to injury. To determine whether PECs change their phenotype upon injury to also express proteins traditionally considered podocyte specific, the following four models of glomerular disease were studied: the transforming growth factor (TGF)-beta1 transgenic mouse model of global glomerulosclerosis, the adriamycin model of focal segmental glomerulosclerosis (FSGS), the anti-glomerular basement membrane (GBM) model of crescentic glomerulonephritis, and the passive Heymann nephritis model of membranous nephropathy. Double immunostaining was performed with antibodies to podocyte-specific proteins (synaptopodin and Wilms' tumor 1) and antibodies to PEC specific proteins (paired box gene 8 and claudin-1). No double staining was detected in normal mice. In contrast, the results showed a statistical increase in the number of cells attached to Bowman basement membrane that were double-positive for both podocyte/PEC proteins in TGF-beta1 transgenic, anti-GBM, and membranous animals. Double-positive cells for both podocyte and PEC proteins were also statistically increased in the glomerular tuft in TGF-beta1 transgenic, anti-GBM, and FSGS mice. These results are consistent with glomerular cells coexpressing podocyte and PEC proteins in experimental glomerular disease, but not under normal circumstances.
authors.affiliation: Division of Nephrology, University of Washington, Seattle, Washington 98195-6521, USA.
authors.forename: Takamoto
authors.initials: T
authors.lastname: Ohse
authors.forename: Michael R
authors.initials: MR
authors.lastname: Vaughan
authors.forename: Jeffrey B
authors.initials: JB
authors.lastname: Kopp
authors.forename: Ronald D
authors.initials: RD
authors.lastname: Krofft
authors.forename: Caroline B
authors.initials: CB
authors.lastname: Marshall
authors.forename: Alice M
authors.initials: AM
authors.lastname: Chang
authors.forename: Kelly L
authors.initials: KL
authors.lastname: Hudkins
authors.forename: Charles E
authors.initials: CE
authors.lastname: Alpers
authors.forename: Jeffrey W
authors.initials: JW
authors.lastname: Pippin
authors.forename: Stuart J
authors.initials: SJ
authors.lastname: Shankland
mesh_terms: D000818:Animals; D019867:Anti-Glomerular Basement Membrane Disease / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D000906:Antibodies; D001323:Autoantibodies; D015415:Biomarkers / Q000378:metabolism; D049109:Cell Proliferation; D004317:Doxorubicin; D004847:Epithelial Cells / Q000378:metabolism* / Q000473:pathology; D005921:Glomerulonephritis / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D015433:Glomerulonephritis, Membranous / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D005923:Glomerulosclerosis, Focal Segmental / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D026541:Heymann Nephritis Antigenic Complex / Q000276:immunology; D007150:Immunohistochemistry; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008822:Mice, Transgenic; D010641:Phenotype; D050199:Podocytes / Q000378:metabolism* / Q000473:pathology; D011506:Proteins / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000378:metabolism
chemical_list: D000906:Antibodies; D001323:Autoantibodies; D015415:Biomarkers; D026541:Heymann Nephritis Antigenic Complex; D011506:Proteins; D053773:Transforming Growth Factor beta1; C051951:antiglomerular basement membrane antibody; D004317:Doxorubicin