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Titolo:
Hyperplastic vascular smooth muscle cells of the intrarenal arteries in angiotensin II type 1a receptor null mutant mice
Autore:
Inokuchi, S; Kimura, K; Sugaya, T; Inokuchi, K; Murakami, K; Sakai, T;
Indirizzi:
Juntendo Univ, Sch Med, Dept Anat, Bunkyo Ku, Tokyo 1138421, Japan Juntendo Univ Tokyo Japan 1138421 Anat, Bunkyo Ku, Tokyo 1138421, Japan Univ Tokyo, Fac Med, Dept Internal Med 2, Tokyo, Japan Univ Tokyo Tokyo Japan okyo, Fac Med, Dept Internal Med 2, Tokyo, Japan Univ Tsukuba, Inst Appl Biochem, Tsukuba, Ibaraki 305, Japan Univ TsukubaTsukuba Ibaraki Japan 305 ochem, Tsukuba, Ibaraki 305, Japan Tanabe Seiyaku Co Ltd, Lead Generat Res Labs, Osaka, Japan Tanabe Seiyaku Co Ltd Osaka Japan , Lead Generat Res Labs, Osaka, Japan Univ Tsukuba, Tsukuba Adv Res Alliance, Tsukuba, Ibaraki 305, Japan Univ Tsukuba Tsukuba Ibaraki Japan 305 iance, Tsukuba, Ibaraki 305, Japan Juntendo Univ, Sch Med, Dept Anat, Tokyo 113, Japan Juntendo Univ Tokyo Japan 113 Univ, Sch Med, Dept Anat, Tokyo 113, Japan
Titolo Testata:
KIDNEY INTERNATIONAL
fascicolo: 2, volume: 60, anno: 2001,
pagine: 722 - 731
SICI:
0085-2538(200108)60:2<722:HVSMCO>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
BLOOD-PRESSURE; DEFICIENT MICE; CONVERTING ENZYME; HYPERTENSIVE RAT; HYPERTROPHY; GENE; HYPERPLOIDY; MIGRATION; FERTILITY; SUBTYPES;
Keywords:
renal artery; hypertrophy; cell signaling; extracellular matrix; renin-angiotensin system; targeted gene deletion; intrarenal vascular structure;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
37
Recensione:
Indirizzi per estratti:
Indirizzo: Inokuchi, S Juntendo Univ, Sch Med, Dept Anat, Bunkyo Ku, 2-1-1 Hongo, Tokyo 1138421, Japan Juntendo Univ 2-1-1 Hongo Tokyo Japan 1138421 1138421, Japan
Citazione:
S. Inokuchi et al., "Hyperplastic vascular smooth muscle cells of the intrarenal arteries in angiotensin II type 1a receptor null mutant mice", KIDNEY INT, 60(2), 2001, pp. 722-731

Abstract

Background. Angiotensin II (Ang II), which contracts vascular smooth muscle cells (VSMCs), has been reported to regulate VSMC growth. Recently formedtransgenic mice without angiotensinogen or Ang II receptors showed vascular alterations. However. it is still unclear how their VSMCs alter. We explored the role of Ang II via the Ang II type 1a receptor (AT1a) in VSMCs in vivo using AT1a null mutant mice. Methods. We analyzed the ultrastructure of the intrarenal arteries in AT1anull mutant mice that were homozygous for a targeted disruption of AT1a receptor gene using light and electron microscopy. Results. The structural changes of the intrarenal arteries in AT1a null mutant mice showed the wall thickening, which in the interlobar. arcuate. andproximal interlobular arteries consisted of two additional populations of VSMCs. on the luminal and abluminal sides of the media. The luminal overpopulation of smooth muscle cells (SMCs) was arranged in a longitudinal direction separated by increased interposed elastic laminae. The abluminal overpopulation of SMCs ran in circumferential directions separated from the main population. The cytological structure of VSMCs in AT1a null mutant mice wassmaller in size, contained more organelles for protein synthesis and secretion than in control mice, and had poorly developed contractile apparatus. Conclusions. The lack of AT1a signaling causes structural abnormalities inthe renal vascular system and transforms the phenotype of VSMCs into cell proliferation, induces the escape of VSMCs from the circular mechanical integrity, and results in increased synthesis of extracellular matrices.

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Documento generato il 01/12/20 alle ore 22:27:00