Analysis Tools
normal phenotype
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• mice are viable, fertile and grossly indistinguishable from wild-type littermates
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Allele Symbol Allele Name Allele ID |
Podxltm2Kmn targeted mutation 2, Kelly M McNagny MGI:5694686 |
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| Summary |
2 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice are viable, fertile and grossly indistinguishable from wild-type littermates
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• isolated primary mouse pulmonary endothelial cells (mECs) display a severely impaired ability to spread on laminin and, to a lesser extent, collagen I coated transwells
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• isolated primary mouse pulmonary endothelial cells (mECs) show a significant increase in static adhesion to fibronectin but not to laminin, collagen (type I or type IV) or gelatin relative to control cells
• however, mECs spread normally when plated on fibronectin-coated transwells
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• 2-fold increase in basal lung vascular permeability, as shown by Evans blue dye vascular leakage assays on naive mice
• additional increase in inflammation-induced lung vascular permeability following intra-tracheal LPS treatment
• however, no detectable changes in the ratio of wet/dry lung weight, in vascular density, or in the frequency and phenotype of endothelial cells relative to controls
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• isolated primary mouse pulmonary endothelial cells (mECs) display a severely impaired ability to spread on laminin and, to a lesser extent, collagen I coated transwells
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• isolated primary mouse pulmonary endothelial cells (mECs) show a significant increase in static adhesion to fibronectin but not to laminin, collagen (type I or type IV) or gelatin relative to control cells
• however, mECs spread normally when plated on fibronectin-coated transwells
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• mislocalization of structural matrix proteins in the lung
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• increase in airspace size upon lung inflation at a fixed pressure with an open thoracic cavity, as shown by increased mean linear intercept (MLI) at 10 weeks but not at 1-3 weeks of age
• however, normal sized airspace and alveolar architecture upon lung inflation with a constant volume under closed chest conditions at 10 weeks of age
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• >30% increase in elastin-free fibrillar collagen fibers in alveolar lung tissue, primarily in larger alveolar spaces
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• density of elastin fiber staining is marginally decreased within lung parenchyma tissue as shown by Gomoris aldehyde fuchsin staining, despite an observed increase in elastin transcript levels
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• increase in mean lung volume upon inflation at constant pressure with an open thoracic cavity at 4 and 10 weeks of age
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• increased total lung and airway resistance under closed chest conditions
• however, no significant alterations in total lung capacity or compliance
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• isolated primary mouse pulmonary endothelial cells (mECs) display a severely impaired ability to spread on laminin and, to a lesser extent, collagen I coated transwells
|
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• isolated primary mouse pulmonary endothelial cells (mECs) show a significant increase in static adhesion to fibronectin but not to laminin, collagen (type I or type IV) or gelatin relative to control cells
• however, mECs spread normally when plated on fibronectin-coated transwells
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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 05/07/2024 MGI 6.23 |
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