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K-ras  is essential for embryogenesis and its mutations are involved in human developmental syndromes and cancer. To determine the consequences of  K-ras  activation in urothelium, we used uroplakin-II (UPK II) promoter driven Cre recombinase mice and generated mice with mutated  Kras G12D   allele in the urothelium ( UPK II-Cre;LSL-K-ras G12D  ). The  UPK II-Cre;LSL-K-ras G12D   mice died neonatally due to lung morphogenesis defects consisting of simplification with enlargement of terminal air spaces and dysmorphic pulmonary vasculature. A significant alteration in epithelial and vascular basement membranes, together with fragmentation of laminin, points to extracellular matrix degradation as the causative mechanism of alveolar and vascular defects. Our data also suggest that altered protease activity in amniotic fluid might be associated with matrix defects in lung of  UPK II-Cre;LSL-K-ras G12  . These defects resemble those observed in early stage human neonatal bronchopulmonary dysplasia (BPD), although the relevance of this new mouse model for BPD study needs further investigation.

Specific Activation of K-RasG12D Allele in the Bladder Urothelium Results in Lung Alveolar and Vascular Defects