Molecular Embryology of the Foregut

Autor: Sandrine Faure, Pascal de Santa Barbara
Přispěvatelé: De Santa Barbara, Pascal, Muscle et pathologies, Université Montpellier 1 (UM1)-IFR3, Université Montpellier 1 (UM1)-Université Montpellier 1 (UM1)-Institut National de la Santé et de la Recherche Médicale (INSERM), Association Française contre les Myopathies, Région Languedoc-Roussillon (Chercheur d'Avenir), Ligue Contre le Cancer (Comité de l'Aude).
Rok vydání: 2011
Předmět:
Pathology
endodermal-mesenchymal interaction
Ectoderm
foregut
MESH: Mice
Knockout

Epithelium
Shh
Mice
Upper Gastrointestinal Tract
0302 clinical medicine
MESH: Gene Expression Regulation
Developmental

MESH: Esophagus
MESH: Animals
Lung
[SDV.BDD]Life Sciences [q-bio]/Development Biology
ComputingMilieux_MISCELLANEOUS
Mice
Knockout

0303 health sciences
Genes
Homeobox

Gastroenterology
Gene Expression Regulation
Developmental

Hindgut
Anatomy
medicine.anatomical_structure
Anal atresia
Endoderm
Tracheoesophageal Fistula
MESH: Body Patterning
medicine.medical_specialty
Epithelial-Mesenchymal Transition
MESH: Mutation
MESH: Esophageal Atresia
Biology
Article
Cell Line
adriomycin
03 medical and health sciences
Esophagus
[SDV.BDD] Life Sciences [q-bio]/Development Biology
medicine
Animals
Humans
Bmp
MESH: Lung
Esophageal Atresia
MESH: Mice
Body Patterning
030304 developmental biology
MESH: Humans
MESH: Genes
Homeobox

[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology
Foregut
Midgut
[SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology
Small intestine
MESH: Cell Line
MESH: Upper Gastrointestinal Tract
Disease Models
Animal

MESH: Epithelium
MESH: Epithelial-Mesenchymal Transition
Mutation
Pediatrics
Perinatology and Child Health

MESH: Tracheoesophageal Fistula
MESH: Disease Models
Animal

030217 neurology & neurosurgery
Zdroj: Journal of Pediatric Gastroenterology and Nutrition
Journal of Pediatric Gastroenterology and Nutrition, Lippincott, Williams & Wilkins, 2011, 52 Suppl 1, pp.S2-3. ⟨10.1097/MPG.0b013e3182105a1a⟩
ISSN: 0277-2116
DOI: 10.1097/mpg.0b013e3182105a1a
Popis: The digestive and respiratory systems have different physiological functions (nutrition, food transit and evacuation for the first; breathing and oxygen supply to the blood for the second) and are generally considered and studied as two independent structures. Nevertheless, although at birth they are separated, they both derive from a common and transient developmental structure, the foregut, which is the anterior part of the gastrointestinal (GI) tract (1). The GI tract is a remarkably complex, three-dimensional, specialized and vital system that is derived from a simple tube-like structure. The vertebrate GI tract includes the luminal digestive system (i.e., esophagus, stomach, intestine and colon, which we will designate on the whole as “gut”) and the GI-tract derivatives (i.e., thyroid, lungs, liver and pancreas). The gut is composed of three germ layers: mesoderm (which forms the smooth muscle layer), endoderm (which forms the epithelial lining) and ectoderm (which includes the enteric nervous system). The gut develops from two invaginations at the anterior (anterior intestinal portal, AIP) and posterior (caudal intestinal portal, CIP) end of the embryo that elongate and fuse to form a straight tube. The primitive gut tube is initially patterned into three broad domains along its anterior-posterior (AP) axis: the fore-, mid- and hindgut. As they develop, each region of the gut is characterized by unique mesodermal and endodermal morphologies, which can easily be discerned by gross and microscopic examination. Specifically, these tissues show regional differentiation along the AP axis that specifies pharynx, esophagus and stomach (the foregut), small intestine (the midgut) and large intestine (hindgut). This regionalization is maintained throughout life and is essential and necessary for normal gut function. These patterning events are remarkably conserved across species (1) and patterning anomalies are likely to be responsible for many of the human gut malformation syndromes, such as tracheo-esophageal atresia (TE), infantile hypertrophic pyloric stenosis or anal atresia (1,2).
Databáze: OpenAIRE