Cycling Werner's syndrome fibroblasts display calcium-dependent potassium currents

R. G.A. Faragher, S. P. Hardy, T. Davis, S. Dropcova, M. C. Allen

Research output: Contribution to journalArticle

Abstract

Werner's Syndrome (WS) fibroblasts undergo premature senescence. Two hypotheses have been proposed to explain this phenomenon: (i) the phenotype is due to the overexpression of senescence-specific proteins in every cell in the population. Such proteins are known to suppress calcium-dependent potassium currents. (ii) The WS mutation greatly increases the proportion of cells that stop cycling at each generation and become senescent. If hypothesis (i) is correct, such currents should be suppressed in all WS fibroblasts; whereas hypothesis (ii) predicts that they will be retained in the cycling fraction of the population. To distinguish between these hypotheses whole-cell patchclamp currents were recorded from cycling cells. Slowly activating outward calcium-dependent potassium currents were detected in both cycling WS and control fibroblasts. These findings support hypothesis (ii): the premature senescence of WS fibroblasts is due to an increased rate of transition from cycling to senescence in the total cell population.

Original languageEnglish
Pages (from-to)119-122
Number of pages4
JournalExperimental Cell Research
Volume231
Issue number1
DOIs
Publication statusPublished - 25 Feb 1997

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Werner Syndrome
Potassium
Fibroblasts
Calcium
Population
Proteins
Phenotype
Mutation

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Cycling Werner's syndrome fibroblasts display calcium-dependent potassium currents. / Faragher, R. G.A.; Hardy, S. P.; Davis, T.; Dropcova, S.; Allen, M. C.

In: Experimental Cell Research, Vol. 231, No. 1, 25.02.1997, p. 119-122.

Research output: Contribution to journalArticle

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T1 - Cycling Werner's syndrome fibroblasts display calcium-dependent potassium currents

AU - Faragher, R. G.A.

AU - Hardy, S. P.

AU - Davis, T.

AU - Dropcova, S.

AU - Allen, M. C.

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AB - Werner's Syndrome (WS) fibroblasts undergo premature senescence. Two hypotheses have been proposed to explain this phenomenon: (i) the phenotype is due to the overexpression of senescence-specific proteins in every cell in the population. Such proteins are known to suppress calcium-dependent potassium currents. (ii) The WS mutation greatly increases the proportion of cells that stop cycling at each generation and become senescent. If hypothesis (i) is correct, such currents should be suppressed in all WS fibroblasts; whereas hypothesis (ii) predicts that they will be retained in the cycling fraction of the population. To distinguish between these hypotheses whole-cell patchclamp currents were recorded from cycling cells. Slowly activating outward calcium-dependent potassium currents were detected in both cycling WS and control fibroblasts. These findings support hypothesis (ii): the premature senescence of WS fibroblasts is due to an increased rate of transition from cycling to senescence in the total cell population.

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