Phenotypes associated with this allele

• Allele Symbol: Gt(ROSA)26Sor^{em117(CAG-Gpld1,-tdTomato)Smoc}
• Allele Name: endonuclease-mediated mutation 117, Shanghai Model Organisms Center
• Allele ID: MGI:7623919
• Summary: 1 genotype

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Gt(ROSA)26Sor^em117(CAG-Gpld1,-tdTomato)Smoc/Gt(ROSA)26Sor^+ Tg(Myh6-cre)2182Mds/0	involves: C57BL/6JSmoc * FVB/N	MGI:8375450

Genotype
MGI:8375450

cn1

• Allelic Composition: Gt(ROSA)26Sor^{em117(CAG-Gpld1,-tdTomato)Smoc}/Gt(ROSA)26Sor⁺; Tg(Myh6-cre)2182Mds/0
• Genetic Background: involves: C57BL/6JSmoc * FVB/N

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

cardiovascular system

abnormal myocardial fiber mitochondrial morphology ( J:379476 )

• upon transverse aortic constriction (TAC) surgery, mice exhibit significantly less mitochondrial structural damage in myocardial tissues than TAC-treated controls

• AAV9-uPAR administration leads to reduced mitochondrial quantity and disrupted mitochondrial morphology in the presence of TAC

decreased response of heart to induced stress ( J:379476 )

• 12-month-old mice subjected to TAC surgery for 4 weeks show attenuated cardiac dysfunction with smaller decreases in global longitudinal strain, less diastolic dysfunction, rescue of TAC-induced reductions in ejection fraction and fractional shortening, less cardiac enlargement, smaller cross-sectional areas of cardiomyocytes, decreased protein levels of hypertrophic markers (NPPA/ANF and MYH7/beta-MHC), and less fibrosis (collagen volume) than TAC-treated controls

• cardiac-specific knockdown of GPLD1 by intramyocardial injection-mediated delivery of AAV9-shGPLD1 abolishes the GPLD1-mediated cardioprotective effect against TAC

• cardiac-specific overexpression of PLAUR/uPAR by intramyocardial injection of AAV9-uPAR prior to TAC surgery does not protect against TAC-induced cardiac dysfunction; morphological and histological analyses show that AAV9-uPAR reduces the beneficial effects of GPLD1 overexpression in response to TAC

homeostasis/metabolism

decreased response of heart to induced stress ( J:379476 )

• 12-month-old mice subjected to TAC surgery for 4 weeks show attenuated cardiac dysfunction with smaller decreases in global longitudinal strain, less diastolic dysfunction, rescue of TAC-induced reductions in ejection fraction and fractional shortening, less cardiac enlargement, smaller cross-sectional areas of cardiomyocytes, decreased protein levels of hypertrophic markers (NPPA/ANF and MYH7/beta-MHC), and less fibrosis (collagen volume) than TAC-treated controls

• cardiac-specific knockdown of GPLD1 by intramyocardial injection-mediated delivery of AAV9-shGPLD1 abolishes the GPLD1-mediated cardioprotective effect against TAC

• cardiac-specific overexpression of PLAUR/uPAR by intramyocardial injection of AAV9-uPAR prior to TAC surgery does not protect against TAC-induced cardiac dysfunction; morphological and histological analyses show that AAV9-uPAR reduces the beneficial effects of GPLD1 overexpression in response to TAC

decreased protein level ( J:379476 )

• mice exhibit a significant decrease in protein levels of PLAUR (plasminogen activator, urokinase receptor; aka uPAR) in cardiac tissues after both sham and TAC surgery

muscle

abnormal myocardial fiber mitochondrial morphology ( J:379476 )

• upon transverse aortic constriction (TAC) surgery, mice exhibit significantly less mitochondrial structural damage in myocardial tissues than TAC-treated controls

• AAV9-uPAR administration leads to reduced mitochondrial quantity and disrupted mitochondrial morphology in the presence of TAC

cellular

abnormal myocardial fiber mitochondrial morphology ( J:379476 )

• upon transverse aortic constriction (TAC) surgery, mice exhibit significantly less mitochondrial structural damage in myocardial tissues than TAC-treated controls

• AAV9-uPAR administration leads to reduced mitochondrial quantity and disrupted mitochondrial morphology in the presence of TAC