Increased neuronal expression of alpha B‐crystallin in human olivary hypertrophy

Fukushima, Kazuko; Mizuno, Yuji; Takatama, Masamitsu; Okamoto, Koichi

doi:10.1111/j.1440-1789.2006.00682.x

Cited by 16 publications

(18 citation statements)

References 23 publications

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“…This is probably attributable to the fact that HspB5 expression initially was not detected in neurons and later only in single "ballooned" neurons under pathological conditions (Iwaki et al 1992 ;Kato et al 1992a , b ;Lowe et al 1992 ). It was also found in neurons after cerebral infarction and olivary hypertrophy (Fukushima et al 2006 ;Minami et al 2003 ). Recently, using cultured hippocampal neurons it could be confi rmed that HspB5 is responsive to several stress conditions, such as heat shock, oxidative, sodium arsenite or hyperosmotic stress in neurons themselves (BarteltKirbach and Golenhofen 2014 ; Kirbach and Golenhofen 2011 ).…”

Section: Cellular Distribution Of Hspb5: Glia Versus Neuronsmentioning

confidence: 90%

HspB5/αB-Crystallin in the Brain

Golenhofen

Bartelt-Kirbach

2015

Heat Shock Proteins

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Many organs including the brain exhibit powerful endogenous cytoprotective mechanisms to survive recurrent cellular stress events, i.e. the development of stress tolerance. Investigation of the molecular mechanisms underlying this neuroprotective phenomenon is of special interest since it may provide the basis to develop new therapeutic strategies for the treatment of neurological diseases. One important mechanism is the upregulation of heat shock proteins. Here, we will review the neuroprotective potential of HspB5/αB-crystallin. HspB5 is expressed in glia as well as in neurons and upregulated in certain cell types or subset of cells at pathophysiological conditions. HspB5 is found to be associated with the diseasecausing pathological protein aggregates, such as amyloid plaques in Alzheimer's disease or Rosenthal fi bers in Alexander disease. One possible function of HspB5 is to counteract the aggregation process leading to increased cell survival. However, HspB5 may act additionally via its non-chaperone functions, such as anti-infl ammatory, anti-apoptotic properties or association with cytoskeletal proteins infl uencing fi lament assembly. The cytoprotective activity of HspB5 is regulated by phosphorylation. Interestingly, in neurons HspB5 is recruited to axons and dendrites by phosphorylation, however, to this end little is known about the molecular targets of phosphoHspB5 in neurons. Identifying the impact of phosphorylation of HspB5 in glia and neurons and the targets of HspB5 may be useful to develop new therapeutic strategies for neurological diseases.

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Section: Cellular Distribution Of Hspb5: Glia Versus Neuronsmentioning

confidence: 90%

HspB5/αB-Crystallin in the Brain

Golenhofen

Bartelt-Kirbach

2015

Heat Shock Proteins

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“…It is a phenomenon observed in adult brains secondary to lesions of the central tegmental tract, red or dentate nuclei that cause deafferentation of the inferior olive [29,30] and is associated with altered synaptophysin reactivity in the hypertrophic inferior olive [31] and strong α-B-crystallin expression [32]. Our study demonstrates that olivary pseudohypertrophy does not occur prior to innervation in the 9-week fetus or during maturation.…”

Section: Discussionmentioning

confidence: 91%

Sequence of Synaptogenesis in the Fetal and Neonatal Cerebellar System - Part 1: Guillain-Mollaret Triangle (Dentato-Rubro-Olivo-Cerebellar Circuit)

Sarnat¹,

Flores‐Sarnat²,

Auer³

2013

Dev Neurosci

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Precise temporal and spatial sequences of synaptogenesis occur in the cerebellar system, as in other synaptic circuits of the brain. In postmortem brain sections of 172 human fetuses and neonates, synaptophysin immunoreactivity was studied in nuclei of the Guillain-Mollaret triangle: dentato-olivo-rubro-cerebellar circuit. Synaptophysin demonstrates not only progressive increase in synaptic vesicles in each structure, but also shows the development of shape from amorphous globular neuronal aggregates to undulated nuclei. Intensity of synaptophysin reactivity is strong before the mature shape of these nuclei is achieved. Accessory olivary and deep cerebellar nuclei are intensely stained earlier than the principal olivary and dentate nuclei. The dorsal blades of both form earlier than the ventral, with reactivity initially peripheral. Initiation of synaptophysin reactivity is at 13 weeks in the inferior olive (r6, r7) and at 16 weeks in the dentate (r2). Initial synaptic vesicles are noted at 13 weeks in the red nucleus (r0); synapses form initially on the small neurons at 13 weeks but thereafter simultaneously on small and large neurons. Form and reactivity follow caudorostral, dorsoventral and mediolateral gradients in the axes of the rhombencephalon. This study provides control data to serve as a basis for interpreting aberrations in synaptogenesis in malformations of the cerebellar system, genetic disorders and acquired insults to the cerebellum and brainstem during fetal life, applicable to tissue sections and complementing biochemical and molecular techniques.

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“…In our preliminary report, 6 we showed αB‐crystallin (αBC)‐positive neurons in PH‐IO for the first time, followed by a report of Fukushima et al. 7 αBC is one of the major components of the ocular lens, 10 and is also one of the small heat shock proteins (HSPs) 11 . In normal brain, αBC is expressed in the oligodendrocytes and astrocytes, but not in neurons 12–14 …”

Section: Introductionmentioning

confidence: 84%

Pathological study of pseudohypertrophy of the inferior olivary nucleus

et al. 2010

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There have been only a few reports about the immunohistochemical study of pseudohypertrophy of the inferior olivary nucleus (PH-IO). We therefore performed the detailed immunohistochemical study of 10 PH-IOs in 8 patients to clarify the mechanism of neuronal degeneration and its related phenomenon of PH-IO. We used various antibodies to alphaB-crystallin (alphaBC), synaptophysin (SYP), microtubule-associated protein 2 (MAP2), Lys-Asp-Glu-Leu (KDEL) receptors, heat shock protein (HSP) 27 as well as SMI-31. We found alphaBC-positive neurons on the ipsilateral side of 10 PH-IOs. SMI-31-positive neurons were also observed in 6 PH-IOs. Confocal laser microscopy showed co-localization of alphaBC and SMI-31 in some neurons. However, there were no HSP27-positive neurons or astrocytes in any of the 10 PH-IOs. MAP2 immunostaining showed MAP2-positive hypertrophic thick neurites around hypertrophic neurons on the ipsilateral side of 7 PH-IOs and demonstrated "glomeruloid structures" in 3 PH-IOs. In addition, fine granular SYP-immunoreactivity was decreased in the neuropils on the ipsilateral side of all 10 PH-IOs. SYP-immunoreactive dots were scattered in the neuropils and on the neuronal cell bodies on the side of 7 PH-IOs, and the aggregation of SYP-immunoreactive dots scattered in the neuropils was shown in 3 PH-IOs. Double-immunostainings using anti-MAP2 and anti-SYP antibodies demonstrated frequent SYP-immunoreactive dots along the MAP2-positive hypertrophic thick neurites and their cell bodies. Periphery-stained KDEL-positive neurons were also found on the side of 7 PH-IOs. We showed that the change of the distribution of presynaptic terminals correlated well to the hypertrophic thick neurites in PH-IO. Our immuohistochemical stainings demonstrated various changes which occurred to the neurons in PH-IO, and their neurites and presynaptic terminals. We considered that alphaBC was expressed in the neurons in PH-IO, induced by cellular stress. Such a detailed immunohistochemical investigation has not been reported previously.

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Increased neuronal expression of alpha B‐crystallin in human olivary hypertrophy

Cited by 16 publications

References 23 publications

HspB5/αB-Crystallin in the Brain

HspB5/αB-Crystallin in the Brain

Sequence of Synaptogenesis in the Fetal and Neonatal Cerebellar System - Part 1: Guillain-Mollaret Triangle (Dentato-Rubro-Olivo-Cerebellar Circuit)

Pathological study of pseudohypertrophy of the inferior olivary nucleus

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