NDLI: Modeling Ca2+ Dynamics of Mouse Cardiac Cells Points to a Critical Role of SERCA's Affinity for Ca2+

Content Provider	PubMed Central
Author	Luc, Raeymaekers Ilse, Vandecaetsbeek Frank, Wuytack Vangheluwe, Peter
Copyright Year	2011
Abstract	The SERCA2a isoform of the sarco/endoplasmic reticulum Ca2+ pumps is specifically expressed in the heart, whereas SERCA2b is the ubiquitously expressed variant. It has been shown previously that replacement of SERCA2a by SERCA2b in mice (SERCA2b/b mice) results in only a moderate functional impairment, whereas SERCA activity is decreased by a 40% lower SERCA protein expression and by increased inhibition by phospholamban. To find out whether the documented kinetic differences in SERCA2b relative to SERCA2a (i.e., a twofold higher apparent Ca2+ affinity, but twofold lower maximal turnover rate) can explain these compensatory changes, we simulated Ca2+ dynamics in mouse ventricular myocytes. The model shows that the relative Ca2+ transport capacity of SERCA2a and SERCA2b depends on the SERCA concentration. The simulations point to a dominant effect of SERCA2b's higher Ca2+ affinity over its lower maximal turnover rate. The results suggest that increased systolic and decreased diastolic Ca2+ levels in unstimulated conditions could contribute to the downregulation of SERCA in SERCA2b/b mice. In stress conditions, Ca2+ handling is less efficient by SERCA2b than by SERCA2a, which might contribute to the observed hypertrophy in SERCA2b/b mice. Altogether, SERCA2a might be a better compromise between performance in basal conditions and performance during β-adrenergic stress.
Related Links	http://dx.doi.org/10.1016/j.bpj.2011.01.024
Ending Page	1225
Page Count	10
Starting Page	1216
File Format	PDF
ISSN	00063495
e-ISSN	15420086
Journal	Biophysical Journal
Issue Number	5
Volume Number	100
Language	English
Publisher	The Biophysical Society
Publisher Date	2011-03-01
Access Restriction	Open
Rights Holder	The Biophysical Society
Subject Keyword	Biophysics Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Biophysics

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