Endonuclease G expression in thalamic reticular nucleus after global cerebral ischemia.
Endonuclease G is a mitochondrial enzyme, known to be translocated to the nucleus after transient focal cerebral ischemia and contribute to DNA degradation. After global cerebral ischemia, delayed cell death is observed in the thalamic reticular nucleus but the mechanisms involved are not well described. The purpose of this study was to identify if Endonuclease G was expressed in the cell nucleus of parvalbumin(+) GABA'ergic neurons in relation to cell death after global cerebral ischemia in the thalamic reticular nucleus. The cell death in male Wister rats were studied from 6 h until 4 days after global cerebral ischemia induced by transient 2-vessel carotid occlusion with hypotension for 15 min. Hematoxylin-eosin staining and immunohistochemistry for Endonuclease G, Parvalbumin and Glial fibrillary acidic protein was performed after the ischemic insult. Eosinophilic neurons and vacuolization of the cytoplasm in parvalbumin(+) neurons were observed 2 days after ischemia. Endonuclease G immunoreactivity increased in the cytoplasm 12 h after ischemia and was translocated to the nucleus of parvalbumin(+) neurons after 24 h. In the nucleus of astroglia, Endonuclease G was expressed after 2 days with an apoptotic-like morphology and the number of Endonuclease G-expressing astroglia increased during the later time points. During the same period the number of parvalbumin(+) neurons decreased. In conclusion, this study has identified that Endonuclease G is translocated from the cytoplasm to the nucleus of neurons and expressed with apoptotic-like morphology in the nucleus of astroglia in the thalamic reticular nucleus after global cerebral ischemia.
Department of Biomedical Sciences, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark. mntrk@vip.cybercity.dk
Marianne
M
Nielsen
Jens
J
Zimmer
Nils Henrik
NH
Diemer
D021581:Active Transport, Cell Nucleus; D000818:Animals; D017209:Apoptosis; D001253:Astrocytes / Q000201:enzymology* / Q000473:pathology; D015415:Biomarkers / Q000032:analysis / Q000378:metabolism; D020520:Brain Infarction / Q000201:enzymology* / Q000473:pathology; D002545:Brain Ischemia / Q000201:enzymology* / Q000473:pathology; D002452:Cell Count; D016923:Cell Death; D003593:Cytoplasm / Q000201:enzymology / Q000473:pathology; D004195:Disease Models, Animal; D004706:Endodeoxyribonucleases / Q000378:metabolism*; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000201:enzymology / Q000209:etiology / Q000473:pathology; D007150:Immunohistochemistry; D007395:Interneurons / Q000201:enzymology / Q000473:pathology; D020646:Intralaminar Thalamic Nuclei / Q000098:blood supply / Q000201:enzymology* / Q000473:pathology; D008297:Male; D009410:Nerve Degeneration / Q000201:enzymology / Q000473:pathology; D010320:Parvalbumins / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D015415:Biomarkers; D005904:Glial Fibrillary Acidic Protein; D010320:Parvalbumins; D005680:gamma-Aminobutyric Acid; D004706:Endodeoxyribonucleases; C052391:endonuclease G