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Titolo:
Angiotensin II signaling and HB-EGF shedding via metalloproteinase in glomerular mesangial cells
Autore:
Uchiyama-Tanaka, Y; Matsubara, H; Nozawa, Y; Murasawa, S; Mori, Y; Kosaki, A; Maruyama, K; Masaki, H; Shibasaki, Y; Fujiyama, S; Nose, A; Iba, O; Hasagawa, T; Tateishi, E; Higashiyama, S; Iwasaka, T;
Indirizzi:
Kansai Med Univ, Dept Med 2, Moriguchi, Osaka 5708507, Japan Kansai Med Univ Moriguchi Osaka Japan 5708507 guchi, Osaka 5708507, Japan Taisho Pharmaceut Co Ltd, Pharmacol Lab, Tokushima, Japan Taisho Pharmaceut Co Ltd Tokushima Japan harmacol Lab, Tokushima, Japan Osaka Univ, Fac Med, Sch Allied Hlth Sci, Dept Biochem, Osaka, Japan OsakaUniv Osaka Japan Sch Allied Hlth Sci, Dept Biochem, Osaka, Japan
Titolo Testata:
KIDNEY INTERNATIONAL
fascicolo: 6, volume: 60, anno: 2001,
pagine: 2153 - 2163
SICI:
0085-2538(200112)60:6<2153:AISAHS>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
GROWTH-FACTOR RECEPTOR; VASCULAR SMOOTH-MUSCLE; PROTEIN-KINASE ACTIVATION; TYROSINE KINASE; TRANSFORMING GROWTH-FACTOR-BETA-1; CARDIAC FIBROBLASTS; COUPLED RECEPTORS; TYPE-2 RECEPTORS; TRANSACTIVATION; EXPRESSION;
Keywords:
angiotensin II; HB-EGF; TGF-beta; fibronectin; mesangial cell; EGF receptor; cell signaling;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
46
Recensione:
Indirizzi per estratti:
Indirizzo: Matsubara, H Kansai Med Univ, Dept Med 2, Moriguchi, Osaka 5708507, Japan Kansai Med Univ Moriguchi Osaka Japan 5708507 5708507, Japan
Citazione:
Y. Uchiyama-Tanaka et al., "Angiotensin II signaling and HB-EGF shedding via metalloproteinase in glomerular mesangial cells", KIDNEY INT, 60(6), 2001, pp. 2153-2163

Abstract

Background. Angiotensin II (Ang II) has been implicated in the developmentof glomerulosclerosis by stimulating fibronectin (FN) synthesis. The processing and release of heparin binding-endothelin growth factor (HB-EGF) are activated by protein kinase C (PKC) and Ca2+ signaling. We studied the roles of HB-EGF and endothelial growth factor (EGF) receptor (EGFR) in Ang II-induced FN expression using mesangial cells. Methods. Mesangial cells were prepared from mouse kidneys by the explant method and cells were used at passages 4 and 5. Results. Ang II stimulated FN mRNA levels dose-dependently with a maximal increase (3.4-fold) after 12 hours of incubation. This action was completely inhibited by PKC inhibitors and slightly blocked by Ca2+ chelating agents. FN mRNA accumulation by Ang II was abolished by tyrosine kinase inhibitors, a specific inhibitor for EGFR (AG1478) and extracellular signal-regulated kinase (ERK) inactivation. Addition of neutralizing anti-HB-EGF antibody,as well as pretreatment with heparin or the metalloproteinase inhibitor batimastat abolished induction of FN expression by Ang II. In mesangial cellsstably transfected with a chimeric construct containing HB-EGF and alkaline phosphatase (ALP) genes, ALP activity in incubation medium was rapidly increased by Ang II (1.7-fold at 0.5 min) and reached a 4.1-fold increase at two minutes. Ang II phosphorylated EGFR (maximal at 2 min) and ERK (maximalat 8 min) in a PKC- and metalloproteinase-dependent manner. Ang II stimulated the expression and release of transforming growth factor-beta (TGF-beta) via EGFR-mediated signaling, and the released TGF-beta also contributed to Ang II-mediated FN expression via EGFR transactivation. Conclusions. Ang II-mediated FN expression was regulated by autocrine effects of HB-EGF and TGF-beta, suggesting a novel paradigm for cross-talk between Ang II and growth factor receptor signaling pathways.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/09/20 alle ore 09:23:02