Astroglial Heme Oxygenase-1 and the Origin of Corpora Amylacea in Aging and Degenerating Neural Tissues
Identifieur interne : 001665 ( Ncbi/Curation ); précédent : 001664; suivant : 001666Astroglial Heme Oxygenase-1 and the Origin of Corpora Amylacea in Aging and Degenerating Neural Tissues
Auteurs : Wei Song [Canada] ; Hillel Zukor [Canada] ; Adrienne Liberman [Canada] ; Sagi Kaduri [Canada] ; Zoe Arvanitakis [États-Unis] ; David A. Bennett [États-Unis] ; Hyman M. Schipper [Canada]Source :
- Experimental neurology [ 0014-4886 ] ; 2014.
Abstract
Corpora amylacea (CA) are glycoproteinaceous (predominantly glial and extracellular) inclusions that accumulate in normal aging brain and, to a greater extent, in Alzheimer disease (AD). Previous pharmacological evidence suggested that up-regulation of endogenous heme oxygenase-1 (HO-1) in astrocytes promotes transformation of normal mitochondria to CA-like inclusions. Here, we determined whether 1)
CA were ascertained in (i) neonatal rat astroglia transfected with flag-tagged human HO-1 cDNA, (ii) brain sections derived from 19 month-old GFAP.HMOX1 and wild-type (WT) mice, and (iii) post-mortem hippocampal sections from individuals with mild (MCI) and no cognitive impairment (NCI) after staining with PAS or antisera against HO-1, ubiquitin (Ub), manganese suoperoxide dismutase (MnSOD), α-synuclein or tyrosine hydroxylase (TH).
HO-1 promotes mitochondrial damage and CA biogenesis in astrocyte cultures and in the intact aging brain. CA formation is enhanced in the MCI hippocampus and thus occurs relatively early in the pathogenesis of AD. Glial HO-1 suppression may attenuate bioenergetic failure and slow disease progression in AD and other neurodegenerative conditions featuring accelerated accumulation of CA.
Url:
DOI: 10.1016/j.expneurol.2014.01.006
PubMed: 24440642
PubMed Central: 4020524
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<front><div type="abstract" xml:lang="en"><sec id="S1"><title>Background</title>
<p id="P2">Corpora amylacea (CA) are glycoproteinaceous (predominantly glial and extracellular) inclusions that accumulate in normal aging brain and, to a greater extent, in Alzheimer disease (AD). Previous pharmacological evidence suggested that up-regulation of endogenous heme oxygenase-1 (HO-1) in astrocytes promotes transformation of normal mitochondria to CA-like inclusions. Here, we determined whether 1) <italic>HMOX1</italic>
transfection fosters the accumulation of CA-like inclusions in cultured rat astroglia; 2) the <italic>HMOX1</italic>
transgene promotes CA formation in the brains of aging GFAP.HMOX1 mice; and 3) brain mitochondrial damage and CA biogenesis are augmented in persons with mild cognitive impairment (MCI), a harbinger of AD.</p>
</sec>
<sec id="S2"><title>Methods</title>
<p id="P3">CA were ascertained in (i) neonatal rat astroglia transfected with flag-tagged human HO-1 cDNA, (ii) brain sections derived from 19 month-old GFAP.HMOX1 and wild-type (WT) mice, and (iii) post-mortem hippocampal sections from individuals with mild (MCI) and no cognitive impairment (NCI) after staining with PAS or antisera against HO-1, ubiquitin (Ub), manganese suoperoxide dismutase (MnSOD), α-synuclein or tyrosine hydroxylase (TH).</p>
</sec>
<sec id="S3"><title>Results</title>
<p id="P4"><italic>HMOX1</italic>
transfection induced cytoplasmic vacuolation and the accumulation of PAS+ inclusions in cultured astroglia. Numerous CA-like inclusions stained with PAS− and immunoreactive for HO-1, Ub and MnSOD were observed in the brains of GFAP.HMOX1 mice, but were rarely encountered in age-matched, wild-type controls. Numbers of HO-1-positive CA were significantly increased in certain hippocampal strata of MCI subjects relative to NCI preparations. MnSOD and Ub proteins co-localized to CA in both the control and MCI specimens.</p>
</sec>
<sec id="S4"><title>Conclusions</title>
<p id="P5">HO-1 promotes mitochondrial damage and CA biogenesis in astrocyte cultures and in the intact aging brain. CA formation is enhanced in the MCI hippocampus and thus occurs relatively early in the pathogenesis of AD. Glial HO-1 suppression may attenuate bioenergetic failure and slow disease progression in AD and other neurodegenerative conditions featuring accelerated accumulation of CA.</p>
</sec>
</div>
</front>
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