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Titolo:
Activation of MAPKs in proximal tubule cells from spontaneously hypertensive and control Wistar-Kyoto rats
Autore:
Parenti, A; Cui, XL; Hopfer, U; Ziche, M; Douglas, JG;
Indirizzi:
Case Western Reserve Univ, Sch Med, Dept Med W165, Div Hypertens, Cleveland, OH 44106 USA Case Western Reserve Univ Cleveland OH USA 44106 Cleveland, OH 44106 USA Case Western Reserve Univ, Sch Med, Dept Physiol & Biophys, Cleveland, OH 44106 USA Case Western Reserve Univ Cleveland OH USA 44106 Cleveland, OH 44106 USA Univ Hosp Cleveland, Cleveland, OH 44106 USA Univ Hosp Cleveland Cleveland OH USA 44106 eland, Cleveland, OH 44106 USA Univ Florence, Dept Pharmacol, Florence, Italy Univ Florence Florence Italy Florence, Dept Pharmacol, Florence, Italy Univ Florence, CIMMBA, Florence, Italy Univ Florence Florence ItalyUniv Florence, CIMMBA, Florence, Italy
Titolo Testata:
HYPERTENSION
fascicolo: 5, volume: 35, anno: 2000,
pagine: 1160 - 1166
SICI:
0194-911X(200005)35:5<1160:AOMIPT>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
ANGIOTENSIN-II RECEPTORS; EPITHELIAL-CELLS; PROTEIN-KINASE; SIGNAL-TRANSDUCTION; NORMOTENSIVE RATS; ANTIPORT ACTIVITY; C-JUN; MUSCLE; KIDNEY; TRANSPORT;
Keywords:
epithelial cells; protein kinases; hypertension, essential; angiotensin II;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Douglas, JG Case Western Reserve Univ, Sch Med, Dept Med W165, Div Hypertens, 10900 Euclid Ave, Cleveland, OH 44106 USA Case Western Reserve Univ 10900 Euclid Ave Cleveland OH USA 44106
Citazione:
A. Parenti et al., "Activation of MAPKs in proximal tubule cells from spontaneously hypertensive and control Wistar-Kyoto rats", HYPERTENSIO, 35(5), 2000, pp. 1160-1166

Abstract

The aim of this study was to test the hypothesis that differences exist inthe activity and/or expression of mitogen-activated protein kinases (MAPKs) between spontaneously hypertensive rats (SHR) and control Wistar-Kyoto rats (WKY) and that these differences may account for the enhanced activity of the Na+/H+ exchanger (NHE) previously observed in the renal proximal tubule of SHR, Therefore, the activities of c-jun N-terminal kinase(1) (JNK(1)), extracellular signal-regulated kinase(1/2) (ERK1/2), and p38 were investigated. A reduced amount of ERK1 and JNK(1) protein was round in renal cortex specimens of SHR as compared with WKY; however, their activities were thesame. To study the cellular basis of this difference, immortalized proximal tubule cell lines were grown on Millicell-CM filter inserts where the cell lines organize as polarized monolayers with separate access to apical andbasolateral compartments. Although basal JNK(1) and ERK1/2 activities werenot significantly different between WKY and SI-IR cells, anisomycin stimulated JNK, activity in WKY cells more than in SHR cells (eg, at 15 minutes 300% versus 30%, respectively). Similarly, angiotensin II increased JNK(1) and ERK1/2 activity in a time- and concentration-dependent manner in WKY cells but not in SHR cells. Western blot analyses showed a deficit in JNK(1) and ERK1 protein in SHR (0.25 and 0.5, respectively, of the levels in WKY cells), although ERK2 and p38 protein levels were the same. These observations suggest that, although angiotensin II activates MAPKs and MAPKs have beenshown to regulate NHE, this regulatory pathway is unlikely to account for the increased activity of NHE in the proximal tubular epithelium of SHR.

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Documento generato il 25/11/20 alle ore 06:38:51