title: Does perinatal asphyxia induce apoptosis in the inner ear?
abstract: Pre- and perinatal asphyxia is known to be an important risk factor in the development of neonatal hearing impairment. This study aims to evaluate the role of apoptosis, which is known to play an essential role in the development of the inner ear structures, in the development of neonatal hearing loss caused by pre- and perinatal asphyxia. Eight temporal bones of six different newborns were included. We performed a morphologic analysis by both light microscopy, and transmission electron microscopy, as well as immunohistochemical staining to detect the cleaved form of caspase 3 as apoptosis marker and Bcl 2 as anti-apoptotic marker. Early and late phases of apoptosis were evidenced by condensation of chromatin (electron-dense, black structure along nuclear membrane) and fragmentation of the nucleus, respectively. Changes in nuclear morphology during apoptosis correlate with cleavage by caspase 3 located downstream of Bcl 2 action. The immunohistochemistry for cleaved caspase 3 showed a particular predilection for the inner and outer hair cells, spiral ganglion cells and the marginal cells of the stria vascularis. The brain of all examined cases did not show signs of apoptosis. In summary, this investigation suggests that apoptosis takes place before brain tissue apoptosis and is probably an earlier event than thought. Apoptosis of the cochlea is known to play an essential role in the development of the inner ear. Additionally, this study shows that apoptosis may play an important role in the development of hearing impairment, caused by pre- and perinatal asphyxia.
authors.affiliation: Department of Otorhinolaryngology, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria. Joachim.Schmutzhard@i-med.ac.at
authors.forename: Joachim
authors.initials: J
authors.lastname: Schmutzhard
authors.forename: Rudolf
authors.initials: R
authors.lastname: Glueckert
authors.forename: Consolato
authors.initials: C
authors.lastname: Sergi
authors.forename: Ilona
authors.initials: I
authors.lastname: Schwentner
authors.forename: Irene
authors.initials: I
authors.lastname: Abraham
authors.forename: Annelies
authors.initials: A
authors.lastname: Schrott-Fischer
mesh_terms: D000328:Adult; D017209:Apoptosis; D001238:Asphyxia Neonatorum / Q000150:complications / Q000378:metabolism / Q000473:pathology*; D016022:Case-Control Studies; D053148:Caspase 3 / Q000378:metabolism; D007758:Ear, Inner / Q000196:embryology / Q000378:metabolism / Q000473:pathology*; D005260:Female; D005865:Gestational Age; D034381:Hearing Loss / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D007231:Infant, Newborn; D007234:Infant, Premature; D008297:Male; D046529:Microscopy, Electron, Transmission; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D013701:Temporal Bone / Q000196:embryology / Q000378:metabolism / Q000473:pathology
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; C505407:CASP3 protein, human; D053148:Caspase 3