Premium
Cardiac‐specific Cre‐recombinase causes a dose‐dependent transient reduction in systolic function
Author(s) -
Smith Grant H,
Hall Michael E,
Stec David E,
Hall John E
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.596.3
Subject(s) - cre recombinase , cardiac function curve , ejection fraction , cardiac output , medicine , endocrinology , stroke volume , cardiology , chemistry , hemodynamics , gene , heart failure , transgene , biochemistry , genetically modified mouse
The Cre‐loxP system is a useful tool to study the physiological effects of gene knockout. We have employed a widely used inducible cardiac‐specific model, α‐Myosin Heavy Chain Mer‐Cre‐Mer, using tamoxifen (TAM) to activate Cre‐recombinase (Cre). Cre positive C57B/J6 mice were exposed to one (n=4), three (n=3), or five (n=7) daily doses of a 1 mg TAM injection. Echocardiography demonstrated no statistically significant differences in systolic function (SF) at baseline as assessed by ejection fraction (EF), fractional shortening (FS), stroke volume, or cardiac output. In mice exposed to five injections, a fall in all determinants of SF was observed 6 days after initiating TAM, but only EF and FS were decreased significantly. SF returned to near baseline measures 10 days after TAM initiation. Heart weight to body weight ratios were 4.45±0.34, 5.05±0.05, and 6.33±0.61 for one, three, and five TAM injections respectively. TAM had no effect on cardiac function in Cre‐negative mice. Thus, an inducible cardiac specific Cre caused a transient decline in SF that was dependent on the number of TAM doses.