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Titolo:
Abnormal tenascin expression in murine autosomal recessive polycystic kidneys
Autore:
Ojeda, JL;
Indirizzi:
Univ Cantabria, Dept Anat & Cell Biol, E-39005 Santander, Spain Univ Cantabria Santander Spain E-39005 ll Biol, E-39005 Santander, Spain
Titolo Testata:
NEPHRON
fascicolo: 3, volume: 82, anno: 1999,
pagine: 261 - 269
SICI:
0028-2766(199907)82:3<261:ATEIMA>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
RENAL CYSTIC-DISEASE; BASEMENT-MEMBRANE; MOUSE KIDNEY; COLLECTING DUCT; TUBULAR CYSTS; CPK MOUSE; PATHOGENESIS; OBSTRUCTION; REGRESSION; TISSUES;
Keywords:
extracellular matrix; cpk cpk mouse; scanning electron microscopy; tubular basement membrane; collecting duct cysts;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Ojeda, JL Fac Med, Dept Anat & Biol Celular, C Cardenal Herrera Oria,S-N, E-39011 Santander, Spain Fac Med C Cardenal Herrera Oria,S-N Santander Spain E-39011 ain
Citazione:
J.L. Ojeda, "Abnormal tenascin expression in murine autosomal recessive polycystic kidneys", NEPHRON, 82(3), 1999, pp. 261-269

Abstract

The mechanisms responsible for renal cyst formation in congenital polycystic kidney disease (PKD) remain unknown. Changes in extracellular matrix (ECM) are regarded as an important pathogenic factor in PKD. Tenascin, an ECM glycoprotein implicated in abnormal growth in adult organs, has not been systematically evaluated in PKD. In this study, tenascin expression was studied by immunohistochemistry in the autosomal recessive polycystic kidneys ofC57BL/6J (cpk/cpk) mice. Scanning electron microscopy was performed to determine the cyst types and their temporal evolution, and to establish correlations with the immunohistochemistry observations. Cystic lesions evolved in three main stages. Initially, the cysts appeared as segmental dilatationsof both proximal and collecting ducts. In the second stage, the collectingduct cysts (CDCs) underwent rapid growth that led to the destruction of all other kidney elements. In the final stage, the CDCs reached their maximumsize and the PKD mice died. Normal differentiated principal cells and three types of intercalated cells were present in the CDC epithelium. In all three stages an intense tenascin expression was detected selectively in the basement membranes of the cysts. In the last stage, an intense tenascin immunoreactivity was also observed in the interstitial fibrotic tissue. The abnormal presence of tenascin in the basement membranes of the cysts suggests that this glycoprotein is implicated in the pathogenesis of the cysts, possibly by stimulating cell proliferation.

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Documento generato il 22/10/20 alle ore 06:24:25