title: The amniotic band syndrome in the rat is associated with the activation of transforming growth factor-β.
abstract: Amniocentesis in rats is associated with different malformations, such as cleft palate and limb deformation, resembling the human congenital amniotic band syndrome (ABS). Despite many human cases reported in the literature, little is known about the mechanisms involved in ABS. This study addressed if the activation of the transforming growth factor-β1 (TGF-β1) pathway is, in part, associated with amniotic band formation and growth restriction induced in rats by amniocentesis, as by a previously published model. For this purpose, quantification of TGF-β1, α-smooth muscle actin, and collagen type I mRNA and protein levels were determined by quantitative PCR and Western blot analysis, respectively, in the fetus, its amniotic membrane, and the uterus of experimental and control rats. We found that TGF-β1 mRNA levels are increased in the fetus and the amniotic membrane at 6 hours, whereas α-smooth muscle actin, phosphorylated Smad3, and collagen type I increased at 48 hours, suggesting that a fibrotic response is induced after the amniotic sac puncture. Furthermore, fetuses had hemorrhages, syndactyly, and amputation of limbs, similar to human ABS.
authors.affiliation: Department of Molecular Biology and Histocompatibility, General Hospital Dr. Manuel Gea González, Secretaría de Salud, Mexico City, Mexico.
authors.forename: Mirza
authors.initials: M
authors.lastname: Romero-Valdovinos
authors.affiliation: Department of Pediatric Surgery, General Hospital Dr. Manuel Gea González, Secretaría de Salud, Mexico City, Mexico.
authors.forename: Alfonso
authors.initials: A
authors.lastname: Galván-Montaño
authors.affiliation: Department of Molecular Biology and Histocompatibility, General Hospital Dr. Manuel Gea González, Secretaría de Salud, Mexico City, Mexico.
authors.forename: Angélica
authors.initials: A
authors.lastname: Olivo-Díaz
authors.affiliation: Department of Ecology of Pathogenic Agents, General Hospital Dr. Manuel Gea González, Secretaría de Salud, Mexico City, Mexico.
authors.forename: Pablo
authors.initials: P
authors.lastname: Maravilla
authors.affiliation: Molecular Physiology Unit, Department of Genomic Medicine, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México e Instituto Nacional de Ciencias Médicas y de la Nutrición Salvador Zubirán, Mexico City, Mexico.
authors.forename: Norma A
authors.initials: NA
authors.lastname: Bobadilla
authors.affiliation: Unit of Vinculation, Faculty of Medicine, Universidad Nacional Autónoma de México en el Instituto Nacional de Medicina Genómica, Mexico City, Mexico.
authors.forename: Felipe
authors.initials: F
authors.lastname: Vadillo-Ortega
authors.affiliation: Department of Microbiology and Parasitology, Faculty of Medicine, Universidad Nacional Autónoma de México, Mexico City, Mexico. Electronic address: flisser@unam.mx.
authors.forename: Ana
authors.initials: A
authors.lastname: Flisser
mesh_terms: D000199:Actins / Q000235:genetics / Q000378:metabolism; D000649:Amniocentesis; D000652:Amniotic Band Syndrome / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D024042:Collagen Type I / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D005317:Fetal Growth Retardation / Q000235:genetics / Q000378:metabolism; D051381:Rats; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000378:metabolism*
chemical_list: D000199:Actins; D024042:Collagen Type I; D053773:Transforming Growth Factor beta1