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Titolo:
Extracellular signal-regulated kinase mediates stimulation of TGF-beta 1 and matrix by high glucose in mesangial cells
Autore:
Isono, M; Iglesias-De la Cruz, MC; Chen, S; Hong, SW; Ziyadeh, FN;
Indirizzi:
Univ Penn, Renal Electrolyte & Hypertens Div, Dept Med, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 Dept Med, Philadelphia, PA 19104 USA Univ Penn, Penn Ctr Mol Studies Kidney Dis, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 idney Dis, Philadelphia, PA 19104 USA
Titolo Testata:
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
fascicolo: 12, volume: 11, anno: 2000,
pagine: 2222 - 2230
SICI:
1046-6673(200012)11:12<2222:ESKMSO>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIVATED PROTEIN-KINASE; TRANSFORMING GROWTH FACTOR-BETA-1; GENE-EXPRESSION; TGF-BETA; DIABETIC RATS; COLLAGEN GENE; MAP-KINASE; AUTOCRINE ACTIVATION; PROXIMAL TUBULE; ANGIOTENSIN-II;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
50
Recensione:
Indirizzi per estratti:
Indirizzo: Ziyadeh, FN Univ Penn, Renal Electrolyte & Hypertens Div, Dept Med, 700 Clin Res Bldg,415 Curie Blvd, Philadelphia, PA 19104 USA Univ Penn 700 Clin Res Bldg,415 Curie Blvd Philadelphia PA USA 19104
Citazione:
M. Isono et al., "Extracellular signal-regulated kinase mediates stimulation of TGF-beta 1 and matrix by high glucose in mesangial cells", J AM S NEPH, 11(12), 2000, pp. 2222-2230

Abstract

High ambient glucose exerts its injurious effects on renal cells through nonenzymatic and enzymatic pathways, including altered signal transduction and upregulation of the transforming growth factor-beta (TGF-beta) system. Extracellular signal-regulated kinase (ERK), a member of the mitogen-activated protein kinase (MAPK) cascade, is activated in mesangial cells cultured in high glucose and in glomeruli of diabetic rats. However, the biologic consequences of ERK activation in the kidney have not been investigated. To clarify the role of ERK activation, mouse mesangial cells were exposed to normal (5.5 mM) or high (25 mM) glucose with or without addition of PD98059, a specific inhibitor of MAPK/ERK kinase (MEK), an upstream kinase activatorof ERK. Cells that were exposed to high glucose exhibited significant increases in ERK activity, TGF-beta1 expression (total protein, mRNA levels, and promoter activity), [H-3]-proline uptake, and alpha1(I) collagen and fibronectin mRNA levels. Treatment with PD98059 (up to 25 muM) significantly inhibited these parameters. In contrast, 25 muM PD98059 had no significant effect on any of the parameters measured in cells that were exposed to normalglucose. Overexpression of MAPK phosphatase CL100 prevented TGF-beta1 promoter activation by high glucose, confirming the involvement of the MEK-ERK pathway in response to high glucose. The conclusion is that activation of ERK in mesangial cells is responsible for high-glucose-induced stimulation of TGF-beta1 and contributes to the increased extracellular matrix expression.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 17:33:27