All Phenotypes Podxl<tm2Kmn> MGI Mouse

decreased lung endothelial cell adhesion ( J:223453 )

• 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

increased lung endothelial cell adhesion ( J:223453 )

• 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

increased vascular permeability ( J:223453 )

• 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

decreased lung endothelial cell adhesion ( J:223453 )

• 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

increased lung endothelial cell adhesion ( J:223453 )

• 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

abnormal lung morphology ( J:223453 )

• mislocalization of structural matrix proteins in the lung

overexpanded pulmonary alveolus ( J:223453 )

• 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

abnormal pulmonary collagen fibril morphology ( J:223453 )

• >30% increase in elastin-free fibrillar collagen fibers in alveolar lung tissue, primarily in larger alveolar spaces

abnormal pulmonary elastic fiber morphology ( J:223453 )

• 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

abnormal lung volume ( J:223453 )

• increase in mean lung volume upon inflation at constant pressure with an open thoracic cavity at 4 and 10 weeks of age

increased airway resistance ( J:223453 )

• increased total lung and airway resistance under closed chest conditions

• however, no significant alterations in total lung capacity or compliance

decreased lung endothelial cell adhesion ( J:223453 )

• 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

increased lung endothelial cell adhesion ( J:223453 )

• 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

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

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

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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