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Titolo:
Hydrogen peroxide increases extracellular matrix mRNA through TGF-beta in human mesangial cells
Autore:
Iglesias-de la Cruz, MC; Ruiz-Torres, P; Alcami, J; Diez-Marques, L; Ortega-Velazquez, R; Chen, S; Rodriguez-Puyol, M; Ziyadeh, FN; Rodriguez-Puyol, D;
Indirizzi:
Univ Penn, Renal Electrolyte & Hypertens Div, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 rtens Div, Philadelphia, PA 19104 USA Univ Alcala de Henares, Dept Physiol, Madrid, Spain Univ Alcala de Henares Madrid Spain enares, Dept Physiol, Madrid, Spain Univ Alcala de Henares, Dept Med, Madrid, Spain Univ Alcala de Henares Madrid Spain de Henares, Dept Med, Madrid, Spain Univ Penn, Penn Ctr Mol Studies Kidney Dis, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 idney Dis, Philadelphia, PA 19104 USA Inst Salud Carlos III, Ctr Biol Fundamental, Madrid, Spain Inst Salud Carlos III Madrid Spain Ctr Biol Fundamental, Madrid, Spain Hosp Principe Asturias, Nephrol Sect, Madrid, Spain Hosp Principe Asturias Madrid Spain turias, Nephrol Sect, Madrid, Spain Hosp Principe Asturias, Res Unit, Madrid, Spain Hosp Principe Asturias Madrid Spain e Asturias, Res Unit, Madrid, Spain
Titolo Testata:
KIDNEY INTERNATIONAL
fascicolo: 1, volume: 59, anno: 2001,
pagine: 87 - 95
SICI:
0085-2538(200101)59:1<87:HPIEMM>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
GROWTH-FACTOR-BETA; REACTIVE OXYGEN METABOLITES; PLATELET-ACTIVATING-FACTOR; COLLAGEN GENE-EXPRESSION; NF-KAPPA-B; TRANSFORMING GROWTH-FACTOR-BETA-1; ANGIOTENSIN-II; FREE-RADICALS; HIGH GLUCOSE; AUTOCRINE ACTIVATION;
Keywords:
oxidative stress; renal fibrosis; glucose oxidase; reactive oxygen species; glomerulosclerosis; tubulointerstitial fibrosis; transforming growth factor-beta;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Iglesias-de la Cruz, MC Univ Penn, Renal Electrolyte & Hypertens Div, 700 Clin Res Bldg,415 Curie Bldg, Philadelphia, PA 19104 USA Univ Penn 700 ClinRes Bldg,415 Curie Bldg Philadelphia PA USA 19104
Citazione:
M.C. Iglesias-de la Cruz et al., "Hydrogen peroxide increases extracellular matrix mRNA through TGF-beta in human mesangial cells", KIDNEY INT, 59(1), 2001, pp. 87-95

Abstract

Background. Reactive oxygen species (ROS) are excessively produced in pathologic states, including many renal diseases. Transforming growth factor-beta (TGF-beta) may mediate renal fibrotic injury, and ROS may act through the TGF-beta pathway to exert a profibrotic effect. Methods. The expression of TGF-beta1 and extracellular matrix (ECM) components were assessed in cultured human mesangial cells (HMCs) incubated with glucose oxidase (GO), an enzyme that continuously generates hydrogen peroxide from glucose. A neutralizing anti-TGF-beta antibody was added to test the hypothesis that hydrogen peroxide acts through activation of the TGF-betapathway to stimulate ECM expression. Results. Northern blot analysis revealed significantly increased steady-state levels of TGF-beta1 and ECM proteins (collagen types I, III, and IV, and fibronectin) by approximately twofold. While no significant effect on mRNA stability after treatment with GO was observed, other studies employing promoter-reporter assays, competitive-quantitative reverse transcription-polymerase chain reaction, mink lung epithelial cell proliferation assay, and TGF-beta1 enzyme-linked immunosorbent assay all demonstrated significant stimulation by GO (>1.5-fold) of TGF-beta1 promoter activity, mRNA level, bioactivity, and protein production, respectively. Catalase pretreatment prevented the GO-induced stimulation of TGF-beta1 mRNA. When incubations were performed with a panselective neutralizing anti-TGF-beta antibody, the GO-stimulated expression of ECM molecules was prevented. Conclusions. GO-induced hydrogen peroxide production induces TGF-beta1 synthesis and thereby increases ECM gene expression in cultured HMCs. These cellular responses may underlie the development and progression of renal diseases characterized by oxidative stress.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 07/07/20 alle ore 05:59:05