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Titolo:
Changes in ion channel expression accompany cell cycle progression of spinal cord astrocytes
Autore:
Macfarlane, SN; Sontheimer, H;
Indirizzi:
Univ Alabama, Dept Neurobiol, Birmingham, AL USA Univ Alabama Birmingham AL USA abama, Dept Neurobiol, Birmingham, AL USA
Titolo Testata:
GLIA
fascicolo: 1, volume: 30, anno: 2000,
pagine: 39 - 48
SICI:
0894-1491(200003)30:1<39:CIICEA>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT HIPPOCAMPAL ASTROCYTES; PROTEIN-KINASE-C; K+-CHANNEL; POTASSIUM CHANNELS; PROGENITOR CELLS; PHARMACOLOGICAL CHARACTERIZATION; INTRACELLULAR SODIUM; NEUROBLASTOMA-CELLS; RETINOIC ACID; PROLIFERATION;
Keywords:
potassium currents; sodium currents; proliferation; membrane potential; flow cytometry;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
56
Recensione:
Indirizzi per estratti:
Indirizzo: Macfarlane, SN 1719 6th Ave S,CIRC 545, Birmingham, AL 35294 USA 1719 6thAve S,CIRC 545 Birmingham AL USA 35294 35294 USA
Citazione:
S.N. Macfarlane e H. Sontheimer, "Changes in ion channel expression accompany cell cycle progression of spinal cord astrocytes", GLIA, 30(1), 2000, pp. 39-48

Abstract

Arrest of spinal cord astrocytes at defined stages of the cell cycle clockcauses significant changes in the expression of voltage-activated Na+ and K+ currents. Arrest of actively proliferating astrocytes in G1/G0 by all-trans-retinoic acid induces premature expression of inwardly rectifying K+ currents (IKIR) typically expressed only in differentiated astrocytes. By contrast, arrest in S phase by ara-C or Aphidicolin leads to a greater than twofold increase in "delayed" outwardly rectifying currents (IKD) and a concomitant decrease in IKIR. Pharmacological blockade of IKD by TEA and 4AP caused proliferating astrocytes to arrest in G0/G1, suggesting that activity of these channels is required for G1/S checkpoint progression. Conversely, in quiescent astrocytes, inhibition of IKIR by 30 mu M BaCl2 led to an increase in astrocyte proliferation and to an increase in the number of cells inS phase from 5% to 26%. These data suggest that a downregulation of K-IR promotes cell cycle progression through the G1/S checkpoint. Blockade of IKIR in actively proliferating cells, however, leads to an accumulation in G2/M, suggesting that reappearance of this current may be critical for progression beyond DNA synthesis. Interestingly, Na+ currents (INa+) are increasedgreater than fourfold in S phase-arrested cells, yet their pharmacologicalblockade by TTX has no effect on cell cycle progression. However, the resting membrane potential of S phase-arrested cells increases profoundly, and manipulation of membrane potential by the application of low concentrationsof ouabain, or reduction of extracellular potassium, induces the accumulation of quiescent astrocytes in S phase of the cell cycle, suggesting that either depolarization or intracellular sodium, or both, play an important role in promoting astrocyte proliferation. GLIA 30.39-48, 2000. (C) 2000 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/07/20 alle ore 14:59:01