The process of ultrastructural changes from nuclei to apoptotic body

Ihara, Tomomi; Yamamoto, T.-A.M; Sugamata, Masao; Okumura, Hiroki; Ueno, Yoshio

doi:10.1007/s004280050272

Cited by 99 publications

(73 citation statements)

References 8 publications

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“…4i,j). These EM features correspond with those of late-stage apoptosis, namely apoptotic body (Ihara et al, 1998). Indeed, GCs clearly undergo apoptosis, as demonstrated by the TUNEL assay, which revealed a signal throughout the granular layer at 6 months ( Fig.…”

Section: Pcs Undergo Dark Degeneration In Afg3l2 Heterozygous Micesupporting

confidence: 70%

Haploinsufficiency ofAFG3L2, the Gene Responsible for Spinocerebellar Ataxia Type 28, Causes Mitochondria-Mediated Purkinje Cell Dark Degeneration

Maltecca¹,

Magnoni²,

Cerri³

et al. 2009

J. Neurosci.

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Paraplegin and AFG3L2 are ubiquitous nuclear-encoded mitochondrial proteins that form hetero-oligomeric paraplegin-AFG3L2 and homo-oligomeric AFG3L2 complexes in the inner mitochondrial membrane, named m-AAA proteases. These complexes ensure protein quality control in the inner membrane, jointly with a chaperone-like activity on the respiratory chain complexes. Despite coassembling in the same complex, mutations of either paraplegin or AFG3L2 cause two different neurodegenerative disorders. Indeed, mutations of paraplegin are responsible for a recessive form of hereditary spastic paraplegia, whereas mutations of AFG3L2 have been recently associated to a dominant form of spinocerebellar ataxia (SCA28). In this work, we report that the mouse model haploinsufficient for Afg3l2 recapitulates important pathophysiological features of the human disease, thus representing the first SCA28 model. Furthermore, we propose a pathogenetic mechanism in which respiratory chain dysfunction and increased reactive oxygen species production caused by Afg3l2 haploinsufficiency lead to dark degeneration of Purkinje cells and cerebellar dysfunction.

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Section: Pcs Undergo Dark Degeneration In Afg3l2 Heterozygous Micesupporting

confidence: 70%

Haploinsufficiency ofAFG3L2, the Gene Responsible for Spinocerebellar Ataxia Type 28, Causes Mitochondria-Mediated Purkinje Cell Dark Degeneration

Maltecca¹,

Magnoni²,

Cerri³

et al. 2009

J. Neurosci.

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“…Some cells were found to contain crescent-shaped spaces (CSS), which are specific features of the apoptotic formation process. 5) In addition, the aforementioned cells had a condensed ultrastructure. The granular perithelial (GP) cells, which are scavenger cells that surround cerebral vessels and plays a role in the BBB, showed signs of apoptosis; furthermore, the GP cytoplasmic granules had degenerated and showed evidence of what appeared to be ultrafine DE particles (Fig.…”

Section: Resultsmentioning

confidence: 99%

Maternal Diesel Exhaust Exposure Damages Newborn Murine Brains

Sugamata

Ihara

Takano

et al. 2006

JOURNAL OF HEALTH SCIENCE

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To examine pathologically the influence of diesel exhaust (DE) exposure on fetal nervous system development, brain tissue (cerebral cortex and hippocampus) was collected from newborn mice whose mothers were exposed to DE during pregnancy. After DE exposure, these brain tissues showed evidence of numerous caspase 3-positive cells (a common enzymatic biomarker of apoptosis). Some cells were found to contain crescent-shaped spaces, which are suggestive of apoptotic processes. Granular perithelial (GP) cells, scavenger cells surrounding cerebral vessels of the blood-brain barrier, showed signs of apoptosis; furthermore, the GP cytoplasmic granules had degenerated and showed evidence of what appeared to be ultrafine, DE particles. Additionally, the swelling of astrocyte endfoot that surround capillaries showed degenerative changes similar to myelin figures. Furthermore, the apoptosis of endothelial cells and stenosis of some capillaries were observed. These findings varied in severity, depended on DE concentration, and were not observed in the control group. These observations suggest that exposure of pregnant mice to DE might carry a risk of cellular atrophy and might affect fetal brain development. Our findings also reveal that inhalation of DE might be hazardous to the general health of fetuses.

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“…Apoptotic appearance was evaluated based on findings of the ultrastructural process into the apoptotic body described in our previous report. 2) In that report, the ultrastructural apoptotic process was divided into four stages and characteristic findings could be observed at each stage. One of these findings is called crescent-shaped spaces.…”

Section: Methodsmentioning

confidence: 99%

Maternal Exposure to Diesel Exhaust Leads to Pathological Similarity to Autism in Newborns

Sugamata

Ihara

Sugamata

et al. 2006

JOURNAL OF HEALTH SCIENCE

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We have already demonstrated many diesel exhaust particles (DEPs) and some damages in brain tissues (cerebral cortex and hippocampus) of newborn mice whose mothers inhaled DE during pregnancy, and these damages have the possibilities to lead to some disorders of nervous system. In this study, we examined pathological effects on newborn brain by DE-exposure to pregnant mice, especially focused on autism. ICR pregnant mice were exposed to DE and some were exposed to clean air as a comparative control. Brain tissues (cerebellum) were obtained from the mice (housed in a clean air) born from DE-exposure and control pregnant mice, and examined with light and electron microscope. To detect apoptosis, the immunohistochemical staining for caspase-3 was performed, especially; the numbers of positive Purkinje cell in cerebellum were compared between DE-exposure and control. In DE-exposure group, numerous caspase-3 positive cells were diffusely observed and the number of positive Purkinje cells was significant large than in control. Electron microscopically, specific features of apoptosis were found in Purkinje cells in the DE-exposure group. These findings indicate that DE-exposure to pregnant mice has a severe impact on fetal brain development and, especially, numerous apoptotic Purkinje cells cause the innate deficiency of them and would involve the pathogenic backing of autism. Our results would give a grave warning that the maternal inhalation of DE is hazardous to fetuses' health and it is possible that these fetal damages carries a great risk of various disorders of nervous system afterward, such as autism.

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The process of ultrastructural changes from nuclei to apoptotic body

Cited by 99 publications

References 8 publications

Haploinsufficiency ofAFG3L2, the Gene Responsible for Spinocerebellar Ataxia Type 28, Causes Mitochondria-Mediated Purkinje Cell Dark Degeneration

Haploinsufficiency ofAFG3L2, the Gene Responsible for Spinocerebellar Ataxia Type 28, Causes Mitochondria-Mediated Purkinje Cell Dark Degeneration

Maternal Diesel Exhaust Exposure Damages Newborn Murine Brains

Maternal Exposure to Diesel Exhaust Leads to Pathological Similarity to Autism in Newborns

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