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Titolo:
Advanced glycation end products (AGEs)-induced expression of TGF-beta 1 issuppressed by a protease in the tubule cell line LLC-PK1
Autore:
Xiang, GS; Schinzel, R; Simm, A; Munch, G; Sebekova, K; Kasper, M; Niwa, T; Schmitz, C; Heidland, A;
Indirizzi:
Univ Wurzburg, Dept Internal Med, D-97080 Wurzburg, Germany Univ WurzburgWurzburg Germany D-97080 al Med, D-97080 Wurzburg, Germany Univ Wurzburg, Inst Physiol Chem, D-97070 Wurzburg, Germany Univ WurzburgWurzburg Germany D-97070 l Chem, D-97070 Wurzburg, Germany Rhein Westfal TH Aachen, Dept Anat & Cell Biol, Aachen, Germany Rhein Westfal TH Aachen Aachen Germany nat & Cell Biol, Aachen, Germany Inst Prevent & Clin Med, Bratislava, Slovakia Inst Prevent & Clin Med Bratislava Slovakia n Med, Bratislava, Slovakia Nagoya Univ Daiko, Med Ctr, Nagoya, Aichi, Japan Nagoya Univ Daiko NagoyaAichi Japan aiko, Med Ctr, Nagoya, Aichi, Japan
Titolo Testata:
NEPHROLOGY DIALYSIS TRANSPLANTATION
fascicolo: 8, volume: 16, anno: 2001,
pagine: 1562 - 1569
SICI:
0931-0509(200108)16:8<1562:AGEP(E>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
GROWTH-FACTOR-BETA; MESANGIAL CELLS; DIABETIC NEPHROPATHY; HIGH GLUCOSE; TGF-BETA; GLYCOSYLATION; DISEASE; RECEPTOR; TISSUE; RAGE;
Keywords:
AGEs; cell proliferation; imidazolone; TGF-beta 1 rnRNA; trypsin and tubule cells;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Heidland, A Univ Wurzburg, Dept Internal Med, Josef Schneider Str 2, D-97080 Wurzburg,Germany Univ Wurzburg Josef Schneider Str 2 Wurzburg Germany D-97080
Citazione:
G.S. Xiang et al., "Advanced glycation end products (AGEs)-induced expression of TGF-beta 1 issuppressed by a protease in the tubule cell line LLC-PK1", NEPH DIAL T, 16(8), 2001, pp. 1562-1569

Abstract

Background. Advanced glycation end products (AGEs) are assumed to play a key role in diabetic nephropathy (DN). Since little is known about their action in tubule cells, we investigated in LLC-PK1 cells: (i) whether AGE-bovine serum albumin (AGE-BSA) affects cell proliferation and expression of transforming growth factor-beta (TGF-beta1); and (ii) whether the AGE-induced effects can be modulated by trypsin due to interference with its binding proteins at the cell surface. Methods. Arrested cells were exposed to vehicle (control), AGE-BSA (19-76 muM) and BSA (38 muM) in the presence or absence of trypsin (0.625-5.0 mug/ml) (2.5 mug/ml) for 24 h. We evaluated cell proliferation by cell count and by [H-3]thymidine incorporation, TGF-beta1 expression by reverse transcription-polymerase chain reaction (RT-PCR), and TGF-beta1 protein by ELISA. In addition, cell accumulation of AGEs was studied by immunohistochemical staining of the AGE imidazolone. Results. AGE-BSA inhibited [H-3]thymidine incorporation, lowered cell number and increased cell protein content as well as TGF-beta1 mRNA and proteinas compared with control and BSA. Immunohistochemical staining revealed a marked intracellular accumulation of the AGE imidazolone. Co-incubation of AGE-BSA with trypsin ameliorated the impaired thymidine incorporation, the decreased cell count and the enhanced cell protein content. TGF-beta1 overexpression was normalized, while TGF-beta1 protein declined insignificantly. Intracellular imidazolone accumulation was strikingly suppressed. Conclusions. In the tubule cell line LLC-PK1, AGE-BSA exerts an antiproliferative effect, most probably due to TGF-beta1 overproduction. The co-administration of trypsin abrogated this alteration, very likely as a result of an interaction with AGE-binding protein(s), which is supported by the decreased intracellular AGE accumulation. These findings may be the starting point for the development of specific proteolytic enzymes to interfere with the interaction between AGEs and their receptors binding proteins.

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Documento generato il 26/05/20 alle ore 05:09:38