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Phenotypes Associated with This Genotype
Genotype
MGI:3763712
Allelic
Composition
Fgf2tm1Doe/Fgf2tm1Doe
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgf2tm1Doe mutation (1 available); any Fgf2 mutation (20 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• left ventricle chamber is increased 10-fold 4 weeks after infarct induction compared to wild-type mice in which dilation is 6-fold
• expansion index at 4 weeks post-infarct induction is twice as much as in wild-type mice
• following infarct induction mice exhibit less cardiomyocyte hypertrophy (4% increase in cross-section area compared to 19% increase in cross-section area in wild-type mice)
• fibroblast proliferation at 4 days and 1 week post-infarct induction is decreased 33% and 59%, respectively, compared to in wild-type mice
• interstitial fibrosis fails to increase as in wild-type mice after infarct induction
• the decline in vascular density declines more dramatically following myocardial infarct induction compared to in wild-type mice (74% versus 25% at week 1 week, 91% versus 75% at 4 weeks)
• following myocardial infarct induction, the average area per vessel is increased 10-fold compared to in wild-type mice (122.9+/-23.4 um2 compared to 38.7+/-7.9 um2 in wild-type mice and these large sinusoidal vessels often lack smooth muscle/pericyte investment
• however, vessel area is unchanged even after myocardial infarct induction
• following infarct induction, left ventricular function is decreased 20% compared to 11% in wild-type mice
• cardiac infarcts fail to undergo scar contraction after 4 weeks as in wild-type mice
• however, there is no difference in infarct composition or initial size

homeostasis/metabolism
• left ventricle chamber is increased 10-fold 4 weeks after infarct induction compared to wild-type mice in which dilation is 6-fold
• expansion index at 4 weeks post-infarct induction is twice as much as in wild-type mice
• following infarct induction mice exhibit less cardiomyocyte hypertrophy (4% increase in cross-section area compared to 19% increase in cross-section area in wild-type mice)
• fibroblast proliferation at 4 days and 1 week post-infarct induction is decreased 33% and 59%, respectively, compared to in wild-type mice
• interstitial fibrosis fails to increase as in wild-type mice after infarct induction
• the decline in vascular density declines more dramatically following myocardial infarct induction compared to in wild-type mice (74% versus 25% at week 1 week, 91% versus 75% at 4 weeks)
• following myocardial infarct induction, the average area per vessel is increased 10-fold compared to in wild-type mice (122.9+/-23.4 um2 compared to 38.7+/-7.9 um2 in wild-type mice and these large sinusoidal vessels often lack smooth muscle/pericyte investment
• however, vessel area is unchanged even after myocardial infarct induction
• following infarct induction, left ventricular function is decreased 20% compared to 11% in wild-type mice
• cardiac infarcts fail to undergo scar contraction after 4 weeks as in wild-type mice
• however, there is no difference in infarct composition or initial size


Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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last database update
03/25/2025
MGI 6.24
The Jackson Laboratory