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Publication : Activin disrupts epithelial branching morphogenesis in developing glandular organs of the mouse.

First Author  Ritvos O Year  1995
Journal  Mech Dev Volume  50
Issue  2-3 Pages  229-45
PubMed ID  7619733 Mgi Jnum  J:24357
Mgi Id  MGI:72104 Doi  10.1016/0925-4773(94)00342-k
Citation  Ritvos O, et al. (1995) Activin disrupts epithelial branching morphogenesis in developing glandular organs of the mouse. Mech Dev 50(2-3):229-45
abstractText  We report that activin profoundly alters epithelial branching morphogenesis of embryonic mouse salivary gland, pancreas and kidney rudiments in culture, indicating that it may play a role as a morphogen during mammalian organogenesis. In developing pancreas and salivary gland rudiments, activin causes severe disruption of normal lobulation patterns of the epithelium whereas follistatin, an activin-binding protein, counteracts the effect of activin. In the kidney, activin delays branching of the ureter bud and reduces the number of secondary branches. TGF-beta induces a pattern of aberrant branching in the ureter bud derived epithelium distinct from that seen for activin. Reverse-transcriptase polymerase chain reaction, Northern hybridization and in situ hybridization analyses indicate that these developing tissues express the mRNA transcripts for activin subunits, follistatin or activin receptors. Our results are suggestive of a potential role for the activin-follistatin system as an intrinsic regulator of epithelial branching morphogenesis during mammalian organogenesis.
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