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Titolo:
Pressure-induced expression of monocyte chemoattractant protein-1 through activation of MAP kinase
Autore:
Suda, T; Osajima, A; Tamura, M; Kato, H; Iwamoto, M; Ota, T; Kanegae, K; Tanaka, H; Anai, H; Kabashima, N; Okazaki, M; Nakashima, Y;
Indirizzi:
Univ Occupat & Environm Hlth, Sch Med, Dept Internal Med 2, Kitakyushu, Fukuoka 8078555, Japan Univ Occupat & Environm Hlth Kitakyushu Fukuoka Japan8078555 8555, Japan
Titolo Testata:
KIDNEY INTERNATIONAL
fascicolo: 5, volume: 60, anno: 2001,
pagine: 1705 - 1715
SICI:
0085-2538(200111)60:5<1705:PEOMCP>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN MESANGIAL CELLS; REMNANT KIDNEY MODEL; SMOOTH-MUSCLE CELLS; EXPERIMENTAL CRESCENTIC GLOMERULONEPHRITIS; FACTOR-KAPPA-B; GROWTH-FACTOR; GENE-EXPRESSION; ENDOTHELIAL-CELLS; SIGNALING PATHWAYS; GLOMERULAR INJURY;
Keywords:
mesangial cells; glomerular hypertension; transfection assay; progressive glomerulosclerosis; mitogen-activated protein; MAP kinase kinase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
48
Recensione:
Indirizzi per estratti:
Indirizzo: Osajima, A Univ Occupat & Environm Hlth, Sch Med, Dept Internal Med 2, 1-1Iseigaoka,Kitakyushu, Fukuoka 8078555, Japan Univ Occupat & Environm Hlth 1-1 Iseigaoka Kitakyushu Fukuoka Japan 8078555
Citazione:
T. Suda et al., "Pressure-induced expression of monocyte chemoattractant protein-1 through activation of MAP kinase", KIDNEY INT, 60(5), 2001, pp. 1705-1715

Abstract

Background. In glomerular hypertension, mesangial cells (MC) are subjectedto at least two physical forces: a high pressure and mechanical stretch. In 5/6 nephrectomized rat, a model of progressive glomerular sclerosis associated with glomerular hypertension, monocyte chemoattractant protein-1 (MCP-1) is expressed in glomeruli, suggesting the possible role of MCP-1 in thepathogenesis of glomerular sclerosis; however, whether pressure directly affects MCP-1 expression remains undetermined. Here we examined the effects of pressure on MCP-1 expression in cultured rat MC and the signal transduction pathways that lead to MCP-1 expression. Methods. Pressure was applied to MC by instilling compressed helium gas into sealed plates. MCP-1 mRNA and protein levels in MC were detected by reverse transcription-polymerase chain reaction (RT-PCR) or Northern blotting and ELISA or Western blotting, respectively. Mitogen-activated protein (MAP)kinase activity was measured with the catalytic activity of p42/p44 MAP kinase and anti-phospho p42/p44 MAP kinase antibody. A transient transfectionassay that specifically modulates MAP kinase kinase (MEK) activity was carried out. Results. MCs subjected to external pressure expressed MCP-1 mRNA rapidly and transiently with the peak level noted at 10 minutes and 80 mm Hg pressure. MCP-1 protein levels in cell lysates and culture medium also significantly increased after pressure loading. Pressure rapidly increased the phosphorylation level and activity of p42/p44 MAP kinase. Treatment of MC with a MAP kinase kinase (MEK) inhibitor, PD98059, suppressed levels of both pressure-induced MAP kinase activities and MCP-1 mRNA expression. The constitutively activated type of MEK1 induced MCP-1 expression (13.7-fold) even in non-pressurized MC. Conclusions. Our results indicate that pressure per se can induce MCP-1 via activation of MAP kinase pathway, suggesting that glomerular hypertensionmight be involved in the progression of renal diseases through the expression of MCP-1 in MC.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/09/20 alle ore 09:22:01