PMID: 9533955May 12, 1998Paper

Epithelium-specific adenoviral transfer of a dominant-negative mutant TGF-beta type II receptor stimulates embryonic lung branching morphogenesis in culture and potentiates EGF and PDGF-AA

Mechanisms of Development
J ZhaoD Warburton

Abstract

Although exogenous transforming growth factor-beta (TGF-beta) is known to inhibit branching morphogenesis in mouse embryonic lungs in culture, whether the principal negative function of endogenous TGF-beta signaling resides in lung epithelium or mesenchyme remains unresolved. A recombinant adenovirus was constructed, containing a mutated human TGF-beta type II receptor with a truncated cytoplasmic kinase domain. We examined whether this dominant-negative receptor could abolish epithelium-specific endogenous TGF-beta signaling. We introduced the recombinant adenovirus into lung explants via intra-tracheal micro-injection. This resulted in over-expression of exogenous truncated TGF-beta type II receptor only in airway epithelium, not in mesenchyme, as assessed by mRNA level and protein localization. Blockade of endogenous TGF-beta receptor signaling in epithelial endoderm by the mutated dominant-negative TGF-beta type II receptor resulted in significant (65%) stimulation of epithelial branching morphogenesis, while exogenous TGF-beta no longer downregulated epithelial PCNA immunoreactivity and surfactant protein C (SP-C) expression. Additionally, the mitogenic responses to epidermal growth factor (EGF) and platelet-derived growth...Continue Reading

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Citations

Oct 11, 2002·The Journal of Pathology·Takuya WatanabeAkira Hishida
Mar 22, 2003·Current Urology Reports·Michael E Levin, Richard N Schlussel
Mar 8, 2000·Mechanisms of Development·D WarburtonW V Cardoso
Jun 1, 1999·Current Opinion in Pediatrics·D Warburton, M K Lee
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