All Phenotypes Tg(MSR1-Plau)1Ddi MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
cx1	Plaur^tm1Jld/Plaur^tm1Jld Tg(MSR1-Plau)1Ddi/0	B6.Cg-Plaur^tm1Jld Tg(MSR1-Plau)1Ddi	MGI:3690230
cx2	Plg^tm1Jld/Plg⁺ Tg(MSR1-Plau)1Ddi/0	B6.Cg-Plg^tm1Jld Tg(MSR1-Plau)1Ddi	MGI:3690232
cx3	Apoe^tm1Unc/Apoe^tm1Unc Tg(MSR1-Plau)1Ddi/0	involves: 129P2/OlaHsd * C57BL/6 * SJL	MGI:3690213
tg4	Tg(MSR1-Plau)1Ddi/0	involves: C57BL/6 * SJL	MGI:3690222

Allelic Composition	Plaur^tm1Jld/Plaur^tm1Jld Tg(MSR1-Plau)1Ddi/0
Genetic Background	B6.Cg-Plaur^tm1Jld Tg(MSR1-Plau)1Ddi

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plaur^tm1Jld mutation (2 available); any Plaur mutation (18 available)
Tg(MSR1-Plau)1Ddi mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

cardiovascular system

cardiac fibrosis ( J:113474 )

• exhibit more fibrosis at 15 weeks of age than single Plaur homozygotes although show a similar degree of fibrosis as seen in single Tg(MSR1-Plau)1Ddi mutants

heart inflammation ( J:113474 )

• exhibit significantly more cardiac macrophages at 15 weeks of age than single Plaur homozygotes, however show a similar accumulation as seen in single Tg(MSR1-Plau)1Ddi mutants

immune system

heart inflammation ( J:113474 )

• exhibit significantly more cardiac macrophages at 15 weeks of age than single Plaur homozygotes, however show a similar accumulation as seen in single Tg(MSR1-Plau)1Ddi mutants

Allelic Composition	Plg^tm1Jld/Plg⁺ Tg(MSR1-Plau)1Ddi/0
Genetic Background	B6.Cg-Plg^tm1Jld Tg(MSR1-Plau)1Ddi

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plg^tm1Jld mutation (2 available); any Plg mutation (5 available)
Tg(MSR1-Plau)1Ddi mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

cardiovascular system

abnormal heart morphology ( J:113474 )

• exhibit significantly less cardiac fibrosis than seen in single Tg(MSR1-Plau)1Ddi mutants and no increase in cardiac macrophage accumulation

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

increased susceptibility to induced morbidity/mortality ( J:102208 )

• die suddenly beginning at around 11 weeks of age when fed an atherogenic diet, compared to no increase in mortality in Apoe homozyous controls

• mutants that die suddenly show myocardial infarcts, stenoses, and total occlusions of proximal coronary arteries

cardiovascular system

abnormal artery morphology ( J:102208 )

• in a longer atherogenic diet study, develop severe occlusive proximal coronary artery disease and extensive myocardial infarcts

increased susceptibility to atherosclerosis ( J:102208 )

• after 10 weeks on an atherogenic diet, exhibit increased atherosclerosis compared to controls (Apoe homozygotes) as indicated by increased intimal area in aortic root sections and sudanophilic area on pinned aortas

• after 10 weeks on an atherogenic diet, exhibit dilated aortic roots and increased medial destruction compared to controls

artery occlusion ( J:101486 , J:102208 )

• develop occlusive coronary artery disease (J:101486)

• in a longer atherogenic diet study, develop severe occlusive proximal coronary artery disease (J:102208)

abnormal heart morphology ( J:101486 )

• exhibit significantly more collagenous scar formation in hearts at 15-weeks of age than single Apoe homozygotes

enlarged heart ( J:101486 )

• hearts are larger than in single Apoe homozygotes at 15, but not 3, weeks of age

heart inflammation ( J:101486 )

• hearts show more inflammatory cells, mostly macrophages, than single Apoe homozygotes

• accumulation of macrophages in hearts occurs as early as 5 weeks of age, before the onset of cardiac fibrosis or occlusive coronary artery disease

immune system

heart inflammation ( J:101486 )

• hearts show more inflammatory cells, mostly macrophages, than single Apoe homozygotes

• accumulation of macrophages in hearts occurs as early as 5 weeks of age, before the onset of cardiac fibrosis or occlusive coronary artery disease

growth/size/body

enlarged heart ( J:101486 )

• hearts are larger than in single Apoe homozygotes at 15, but not 3, weeks of age

Allelic Composition	Tg(MSR1-Plau)1Ddi/0
Genetic Background	involves: C57BL/6 * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(MSR1-Plau)1Ddi mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

cardiovascular system

enlarged heart ( J:101486 )

• hearts are more massive when fed the Western-type diet beginning at 5 weeks of age compared to controls, however do not develop atherosclerosis or show early mortality

cardiac fibrosis ( J:101486 )

• develop greater cardiac fibrosis than controls when fed a Western-type or normal chow diet

heart inflammation ( J:101486 )

• develop greater cardiac macrophage accumulation than controls when fed a Western-type or normal chow diet

immune system

heart inflammation ( J:101486 )

• develop greater cardiac macrophage accumulation than controls when fed a Western-type or normal chow diet

growth/size/body

enlarged heart ( J:101486 )

• hearts are more massive when fed the Western-type diet beginning at 5 weeks of age compared to controls, however do not develop atherosclerosis or show early mortality

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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