Increased Sarcoplasmic Reticulum Calcium Leak but Unaltered Contractility by Acute CaMKII Overexpression in Isolated Rabbit Cardiac Myocytes
Population
Isolated adult rabbit ventricular myocytes
Comparison
Acute overexpression of CaMKIIdeltaC using… vs LacZ expressing myocytes
Design
Preclinical
Authors
Discussion
Loading...
Member takes
Implication
Alters Ca2+ handling in isolated myocytes; hypothesis-generating for CaMKII arrhythmogenesis, requires in vivo confirmation.
Key Points
- This research examines how acute overexpression of CaMKIIdeltaC affects calcium handling in cardiac myocytes.
- Acute overexpression of CaMKIIdeltaC using adenovirus in isolated adult rabbit ventricular myocytes.
- Assessment of twitch contraction amplitude, kinetics, and calcium current (ICa).
- Analysis of Ca2+ spark frequency and ryanodine receptor phosphorylation levels.
- Increased basal twitch contraction kinetics without changes in amplitude measured at 1 Hz.
- Calcium spark frequency increased by 88% (P<0.05) and fractional SR Ca2+ release increased by 60% (P<0.05).
- Ryanodine receptor phosphorylation at Ser2809 and Ser2815 increased, but FKBP12.6 interaction remained unchanged.
Structured PICO
P
Population
Isolated adult rabbit ventricular myocytes
I
Intervention
Acute overexpression of CaMKIIdeltaC using adenovirus-mediated gene transfer
C
Comparator
LacZ expressing myocytes
O
Outcome
Sarcoplasmic reticulum (SR) Ca2+ leak and contractility (basal twitch contraction amplitude and kinetics)surrogate
Acute CaMKIIdeltaC overexpression in rabbit ventricular myocytes alters RyR function, leading to enhanced SR Ca2+ leak and reduced SR Ca2+ content without reducing twitch contraction.
Cite This Study
Kohlhaas et al. (2005) studied this question.