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Erratum : The enhanced contractility of the phospholamban-deficient mouse heart persists with aging (Journal of Molecular and Cellular Cardiology (2001) 33 (p. 1031-1040))

Slack, J. P.; Grupp, I. L.; Dash, R.; Holder, D.; Schmidt, A. LU ; Gerst, M. J.; Tamura, T.; Tilgmann, C. LU ; James, P. F. LU and Johnson, R., et al. (2001) In Journal of Molecular and Cellular Cardiology 33(7). p.1387-1387
Abstract
The Enhanced Contractility of the Phospholamban-deficient Mouse Heart Persists with Aging. Journal of Molecular and Cellular Cardiology (2001) 33, 1031-1040. Phospholamban ablation in the mouse is associated with significant increases in cardiac contractility. To determine whether this hyperdynamic function persists through the aging process, a longitudinal examination of age-matched phospholamban-deficient and wild-type mice was employed. Kaplan-Meier survival curves indicated no significant differences between phospholamban-deficient and wild-type mice over the first year. Examination of cardiac function revealed significant increases in the rates of contraction (+dP/dt) and relaxation (-dP/dt) in phospholamban-deficient hearts compared... (More)
The Enhanced Contractility of the Phospholamban-deficient Mouse Heart Persists with Aging. Journal of Molecular and Cellular Cardiology (2001) 33, 1031-1040. Phospholamban ablation in the mouse is associated with significant increases in cardiac contractility. To determine whether this hyperdynamic function persists through the aging process, a longitudinal examination of age-matched phospholamban-deficient and wild-type mice was employed. Kaplan-Meier survival curves indicated no significant differences between phospholamban-deficient and wild-type mice over the first year. Examination of cardiac function revealed significant increases in the rates of contraction (+dP/dt) and relaxation (-dP/dt) in phospholamban-deficient hearts compared with their wild-type counterparts at 3, 6, 12, 18 and 24 months of age. Quantitative immunoblotting indicated that the expression levels of the sarcoplasmic reticulum Ca(2+)-ATPase were not altered in wild-type hearts, while they were significantly decreased at 12 months (40%) and 18 months (20%) in phospholamban-deficient hearts. These findings on the persistence of hyperdynamic cardiac function over the long term suggest that phospholamban may constitute an important target for treatment in heart disease (Less)
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published
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keywords
Aging, Ca2+-binding protein, myocardial contraction, Phospholamban
in
Journal of Molecular and Cellular Cardiology
volume
33
issue
7
pages
1 pages
publisher
Elsevier
external identifiers
  • Scopus:0034964232
ISSN
0022-2828
language
English
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yes
id
aab6da74-e6f7-4f65-90f4-cbc7c28bbcf9
date added to LUP
2016-04-11 13:15:30
date last changed
2016-08-30 12:38:52
@misc{aab6da74-e6f7-4f65-90f4-cbc7c28bbcf9,
  abstract     = {The Enhanced Contractility of the Phospholamban-deficient Mouse Heart Persists with Aging. Journal of Molecular and Cellular Cardiology (2001) 33, 1031-1040. Phospholamban ablation in the mouse is associated with significant increases in cardiac contractility. To determine whether this hyperdynamic function persists through the aging process, a longitudinal examination of age-matched phospholamban-deficient and wild-type mice was employed. Kaplan-Meier survival curves indicated no significant differences between phospholamban-deficient and wild-type mice over the first year. Examination of cardiac function revealed significant increases in the rates of contraction (+dP/dt) and relaxation (-dP/dt) in phospholamban-deficient hearts compared with their wild-type counterparts at 3, 6, 12, 18 and 24 months of age. Quantitative immunoblotting indicated that the expression levels of the sarcoplasmic reticulum Ca(2+)-ATPase were not altered in wild-type hearts, while they were significantly decreased at 12 months (40%) and 18 months (20%) in phospholamban-deficient hearts. These findings on the persistence of hyperdynamic cardiac function over the long term suggest that phospholamban may constitute an important target for treatment in heart disease},
  author       = {Slack, J. P. and Grupp, I. L. and Dash, R. and Holder, D. and Schmidt, A. and Gerst, M. J. and Tamura, T. and Tilgmann, C. and James, P. F. and Johnson, R. and Gerdes, A. M. and Kranias, E. G.},
  issn         = {0022-2828},
  keyword      = {Aging,Ca2+-binding protein,myocardial contraction,Phospholamban},
  language     = {eng},
  number       = {7},
  pages        = {1387--1387},
  publisher    = {ARRAY(0xb083388)},
  series       = {Journal of Molecular and Cellular Cardiology},
  title        = {Erratum : The enhanced contractility of the phospholamban-deficient mouse heart persists with aging (Journal of Molecular and Cellular Cardiology (2001) 33 (p. 1031-1040))},
  volume       = {33},
  year         = {2001},
}