title: HSP110, caspase-3 and -9 expression in physiological apoptosis and apoptosis induced by in vivo embryonic exposition to all-trans retinoic acid or irradiation during early mouse eye development.
abstract: Apoptosis is an essential physiological process in embryonic development. In the developing eye of vertebrates, three periods of developmental apoptosis can be distinguished: early, intermediate and later. Within the apoptosis pathway, caspases play a crucial role. It has also been shown that HSP110 may have a potential role in apoptosis. The aim of this research was to study the expression of HSP110, caspase-3 and -9 in physiological, retinoic- or irradiation-induced apoptosis during early eye development. Seven pregnant C57Bl/6J mice received 80 mg kg(-1) of all-trans retinoic acid mixed with sesame oil. Seven pregnant NMRI mice received 2 Gy irradiation at the same gestational day. Control mice of both strains (seven mice of each) were not submitted to any treatment. Embryos were harvested at 3, 6, 12 and 24 h after exposition, fixed, dehydrated and embedded. Coronal sections (5 microm) were made. Slide staining occurred alternatively using anti-caspase-3, anti-caspase-9 and anti-HSP110 immunohistochemistry. HSP110 and caspase-3 expression presented similar topographic and chronological patterns, whereas expression of HSP110 was more precocious in retinoic acid-treated embryos. After retinoic exposure, caspase-3- and HSP110-positive cells were increased in the region of the optic vesicle. By contrast, after irradiation, caspase-3- and HSP110-positive cells were noticeably increased in the optic vesicle, peri-optical mesoderm but less in lens placode. HSP110 was expressed before caspase-3. By contrast, caspase-9 was expressed by a very small number of cells in the optic vesicle either under physiological or under teratogenic conditions. Thus, it seems that activation of caspase-9 is dispensable in early eye developmental apoptosis.
authors: Department of Anatomy and Embryology, Université Libre de Bruxelles, Faculty of Medicine, Brussels, Belgium.
authors: Julien
authors: J
authors: Gashegu
authors: Reza
authors: R
authors: Ladha
authors: Nathalie
authors: N
authors: Vanmuylder
authors: Catherine
authors: C
authors: Philippson
authors: Françoise
authors: F
authors: Bremer
authors: Marcel
authors: M
authors: Rooze
authors: Stéphane
authors: S
authors: Louryan
mesh_terms: D000014:Abnormalities, Drug-Induced / Q000378:metabolism; D000016:Abnormalities, Radiation-Induced / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000528:radiation effects; D053148:Caspase 3 / Q000032:analysis*; D053453:Caspase 9 / Q000032:analysis*; D047108:Embryonic Development / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D005123:Eye / Q000187:drug effects / Q000196:embryology* / Q000528:radiation effects; D005260:Female; D005865:Gestational Age; D050957:HSP110 Heat-Shock Proteins / Q000032:analysis*; D007150:Immunohistochemistry; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D023421:Models, Animal; D011247:Pregnancy; D013723:Teratogens / Q000494:pharmacology; D014212:Tretinoin / Q000494:pharmacology
chemical_list: D050957:HSP110 Heat-Shock Proteins; D013723:Teratogens; D014212:Tretinoin; D053148:Caspase 3; D053453:Caspase 9