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Titolo:
Renal interstitial fibrosis is reduced in angiotensin II type 1a receptor-deficient mice
Autore:
Satoh, M; Kashihara, N; Yamasaki, Y; Maruyama, K; Okamoto, K; Maeshima, Y; Sugiyama, H; Sugaya, T; Murakami, K; Makino, H;
Indirizzi:
Kawasaki Med Sch, Dept Internal Med, Div Nephrol, Kurashiki, Okayama 7010192, Japan Kawasaki Med Sch Kurashiki Okayama Japan 7010192 , Okayama 7010192, Japan Okayama Univ, Sch Med, Dept Med 3, Okayama 700, Japan Okayama Univ Okayama Japan 700 , Sch Med, Dept Med 3, Okayama 700, Japan Tanabe Seiyaku Co Ltd, Discovery Res Lab, Osaka, Japan Tanabe Seiyaku Co Ltd Osaka Japan Ltd, Discovery Res Lab, Osaka, Japan Univ Tsukuba, Tsukuba Adv Res Alliance, Inst Appl Biochem, Tsukuba, Ibaraki 305, Japan Univ Tsukuba Tsukuba Ibaraki Japan 305 ochem, Tsukuba, Ibaraki 305, Japan
Titolo Testata:
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
fascicolo: 2, volume: 12, anno: 2001,
pagine: 317 - 325
SICI:
1046-6673(200102)12:2<317:RIFIRI>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
UNILATERAL URETERAL OBSTRUCTION; KAPPA-B ACTIVATION; GROWTH-FACTOR BETA-1; TUBULOINTERSTITIAL FIBROSIS; CONVERTING ENZYME; RAT-KIDNEY; EXPRESSION; NEPHROPATHY; CHEMOATTRACTANT; INHIBITION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Kashihara, N Kawasaki Med Sch, Dept Internal Med, Div Nephrol, 577 Matsushima, Kurashiki, Okayama 7010192, Japan Kawasaki Med Sch 577 Matsushima Kurashiki Okayama Japan 7010192
Citazione:
M. Satoh et al., "Renal interstitial fibrosis is reduced in angiotensin II type 1a receptor-deficient mice", J AM S NEPH, 12(2), 2001, pp. 317-325

Abstract

Unilateral ureteral obstruction (UUO) results in tubulointerstitial fibrosis of the affected kidney by stimulating the renin-angiotensin system. Thisstudy established a UUO model in angiotensin type 1a receptor (AT1a) deficient (mutant) mice to elucidate the role of angiotensin II through AT1a on the fibrosis of the obstructed kidney (OBK). The relative volume of the tubulointerstitium was measured by an image analyzer; deposition of collagen types III and IV and monocyte/macrophage infiltration were histologically examined using specific antibodies. Also determined were the mRNA levels of transforming growth factor-beta by Northern blot analysis. Nuclear factor-kappa beta activity was assessed by gel shift assay. UUO in wild mice resulted in a marked expansion of relative volume of the tubulointerstitium, together with increased deposition of collagen types III and IV and number of infiltrated monocytes/macrophages in the interstitium, relative to sham-operated mice. In comparison, these changes were significantly lower in mutant mice with UUO. The mRNA level of transforming growth factor-beta was significantly higher in the OBK of wild mice with UUO compared with sham-operated mice. In contrast, the increase in mRNA level in the OBK of mutant mice wassignificantly less than in wild mice. Finally, UUO resulted in activation of nuclear factor-kappa beta in wild mice but was inhibited in the OBK of mutant mice. The results provide direct evidence that angiotensin II acting via the AT1a plays a pivotal role in the development of tubulointerstitial fibrosis in UUO.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/09/20 alle ore 00:22:21