Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Enhanced proliferation of lymphoblasts from patients with Alzheimer dementia associated with calmodulin-dependent activation of the Na+/H+ exchanger
Autore:
Urcelay, E; Ibarreta, D; Parrilla, R; Ayuso, MS; Martin-Requero, A;
Indirizzi:
CSIC, Ctr Invest Biol, Dept Pathophysiol & Human Mol Genet, Madrid 28006, Spain CSIC Madrid Spain 28006 hophysiol & Human Mol Genet, Madrid 28006, Spain
Titolo Testata:
NEUROBIOLOGY OF DISEASE
fascicolo: 2, volume: 8, anno: 2001,
pagine: 289 - 298
SICI:
0969-9961(200104)8:2<289:EPOLFP>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
GROWTH-FACTORS; IMMORTALIZED LYMPHOBLASTS; CYTOPLASMIC PH; ESSENTIAL-HYPERTENSION; MOLECULAR-CLONING; INTRACELLULAR PH; DISEASE PATIENTS; ANTIPORTER; CALCIUM; CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Urcelay, E CSIC, Ctr Invest Biol, Dept Pathophysiol & Human Mol Genet, Velazquez 144,Madrid 28006, Spain CSIC Velazquez 144 Madrid Spain 28006 144,Madrid 28006, Spain
Citazione:
E. Urcelay et al., "Enhanced proliferation of lymphoblasts from patients with Alzheimer dementia associated with calmodulin-dependent activation of the Na+/H+ exchanger", NEUROBIOL D, 8(2), 2001, pp. 289-298

Abstract

We have recently reported that lymphoblasts from late onset Alzheimer's disease (AD) patients show distinct intracellular pH homeostatic features than those obtained from age-matched healthy donors. Here we report that another distinct feature of AD lymphoblasts is their increased rate of proliferation in serum containing medium, suggesting a different responsiveness of AD cells to serum activators. The increased proliferation of AD cells was accompanied by intracellular alkalinization and was prevented by blockers of the plasma membrane Na+/H+ antiporter (NHE), indicating that the exchanger had to be activated to elicit the cellular responses. The activity of this exchanger can be controlled through several signaling pathways, but only the inhibition of calmodulin activity impeded the serum-induced intracellularalkalinization and enhanced proliferation of AD cells. In contrast, the inhibition of calmodulin did not alter the rate of proliferation of normal cells. Thus, it seems plausible to conclude that the enhanced proliferation of AD cells is the result of a surface receptor-mediated activation of the Ca2+-caamoduuln signaling pathway. Our observations add further support in favor that AD may be considered a systemic disease which underlying etiopathogenic mechanism may be an altered responsiveness to cell activating agents. Thus, the use of lymphoblastoid cells from AD patients may be a useful model to investigate cell biochemical aspects of this disease. (C) 2001 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 15:12:07