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Volume 136, Issue 7, Pages 2074-2091 (June 2009)


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The Role of the Visceral Mesoderm in the Development of the Gastrointestinal Tract

Valérie A. McLinCorresponding Author Informationemail address, Susan J. Henning, Milan Jamrich§

Received 19 September 2008; accepted 4 March 2009. published online 19 March 2009.

The gastrointestinal (GI) tract forms from the endoderm (which gives rise to the epithelium) and the mesoderm (which develops into the smooth muscle layer, the mesenchyme, and numerous other cell types). Much of what is known of GI development has been learned from studies of the endoderm and its derivatives, because of the importance of epithelial biology in understanding and treating human diseases. Although the necessity of epithelial-mesenchymal cross talk for GI development is uncontested, the role of the mesoderm remains comparatively less well understood. The transformation of the visceral mesoderm during development is remarkable; it differentiates from a very thin layer of cells into a complex tissue comprising smooth muscle cells, myofibroblasts, neurons, immune cells, endothelial cells, lymphatics, and extracellular matrix molecules, all contributing to the form and function of the digestive system. Understanding the molecular processes that govern the development of these cell types and elucidating their respective contribution to GI patterning could offer insight into the mechanisms that regulate cell fate decisions in the intestine, which has the unique property of rapid cell renewal for the maintenance of epithelial integrity. In reviewing evidence from both mammalian and nonmammalian models, we reveal the important role of the visceral mesoderm in the ontogeny of the GI tract.

John P. Lynch and David C. Metz, Section Editors

 Department of Pediatrics, Section of Gastroenterology, Hepatology and Nutrition, Baylor College of Medicine, Houston, Texas

§ Department of Cellular and Molecular Biology, Baylor College of Medicine, Houston, Texas

 Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas

 Departments of Medicine and Cell and Molecular Physiology, University of North Carolina Chapel Hill, Chapel Hill, North Carolina

Corresponding Author InformationReprint requests Address requests for reprints to: Valérie A. McLin, MD, Unite de Gastroenterologie, Hepatologie et Nutrition Pediatrique, Hopital des Enfants, CH-1211 Geneva, Switzerland

 Conflicts of interest The authors disclose no conflicts.

 Funding V.A.M. is supported by the National Institutes of Health (K08DK078656) and a Young Investigator Award from the Children's Digestive Health and Nutrition Foundation, S.J.H. is supported by the National Institutes of Health (R01DK069585), and M.J. is supported by the Retinal Research Foundation.

PII: S0016-5085(09)00370-9

doi:10.1053/j.gastro.2009.03.001


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