Aging‐related changes in astrocytes in the rat retina: imbalance between cell proliferation and cell death reduces astrocyte availability

Hussein, M. A.; Chamberlain, Coral G.; Weible, Michael; Hughes, Suzanne; Chu, Yi; Chan‐Ling, Tailoi

doi:10.1111/j.1474-9726.2008.00402.x

Cited by 66 publications

(55 citation statements)

References 88 publications

(139 reference statements)

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“…48 A previous study reported that the complicated processes of retinal astrocytes was observed as an aging sign of rat retina. 54 However, the enlargement of the endfeet of retinal astrocytes around blood vessels was much more often observed in the aged TET-1 mice than in the aged Non-tg mice, suggesting an effect of overexpressed ET-1 on astrocytes in our study. One of the possibilities of this phenomenon is end-feet edema, which may suggest the functional deficiency of BRB in the TET-1 mice.…”

Section: Relationship Of Tet-1 Mice With Ntg and Other Vascular-relatcontrasting

confidence: 52%

Progressive Retinal Degeneration in Transgenic Mice with Overexpression of Endothelin-1 in Vascular Endothelial Cells

Mi¹,

Zhang²,

Qian³

et al. 2012

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. Endothelin-1 (ET-1), synthesized in vascular endothelial cells, is a potent vasoconstrictor. ET-1-related vascular abnormality has been known to be important in the pathogenesis of glaucoma, especially in normal tension glaucoma. However, the long-term effect of increased vascular ET-1 on the retinal tissue is still unclear.METHODS. The mice with overexpression of ET-1 in vascular endothelial cells (TET-1 mice) were examined with the profile of intraocular pressure (IOP), retinal layer thickness, numbers of retinal ganglion cells (RGCs), and axonal changes associated with blood vessel changes.RESULTS. The TET-1 mice exhibited a significant progressive loss of RGCs and decrease of retinal thickness in the inner nuclear layer (INL) and outer nuclear layer (ONL) as early as around 10-12 months. At 24 months, the retinal degeneration became more severe, with around 30% RGC loss associated with thinning of the retinal nerve fiber layer and there was an increase in neuronal loss and thinning of the INL and ONL. In the 24-month-old TET-1 mice, IgG leakage in the blood vessels and decrease in the occludin protein were observed. There was increased glial fibrillary acidic protein expression in the Müller cells. In addition, the astrocytic end-feet on blood vessels were enlarged. The IOP level was normal in all ages (1-24 months) of TET-1 mice.CONCLUSIONS. These data suggested that TET-1 mice may be a useful model to address endothelial ET-1-related mechanisms in vascular-associated retinal degenerative diseases. (Invest Ophthalmol Vis Sci. 2012;53:4842-4851)

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Section: Relationship Of Tet-1 Mice With Ntg and Other Vascular-relatcontrasting

confidence: 52%

Progressive Retinal Degeneration in Transgenic Mice with Overexpression of Endothelin-1 in Vascular Endothelial Cells

Mi¹,

Zhang²,

Qian³

et al. 2012

Invest. Ophthalmol. Vis. Sci.

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“…For example, in rat retinal preparations, aging was associated with a decrease in the total number of astrocytes and with an increase in the proportion of cells with gliotic morphology. 159,160 Conversely, a rather significant (by one third) increase in the number of astrocytes was observed in hippocampus of female B57 mice 161 ; similar age-dependent increase in astrocytes quantity was found in the CA1 hippocampal area and in the frontal cortex of male Sprague-Dawley rats; this was accompanied with hypertrophic remodeling that was more prominent in the cortex. 162 An increase (by ϳ20%) in the number of astrocytes was detected in parietal cortex and the dentate gyrus of old Wistar rats.…”

Section: Morphology and Numbersmentioning

confidence: 63%

Astrocytes in Alzheimer's Disease

et al. 2010

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Summary:The circuitry of the human brain is formed by neuronal networks embedded into astroglial syncytia. The astrocytes perform numerous functions, providing for the overall brain homeostasis, assisting in neurogenesis, determining the micro-architecture of the grey matter, and defending the brain through evolutionary conserved astrogliosis programs.Astroglial cells are engaged in neurological diseases by determining the progression and outcome of neuropathological process. Astrocytes are specifically involved in various neurodegenerative diseases, including Alzheimer's disease, amyotrophic lateral sclerosis, Parkinson's disease, and various forms of dementia. Recent evidence suggest that early stages of neurodegenerative processes are associated with atrophy of astroglia, which causes disruptions in synaptic connectivity, disbalance in neurotransmitter homeostasis, and neuronal death through increased excitotoxicity. At the later stages, astrocytes become activated and contribute to the neuroinflammatory component of neurodegeneration.

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“…*p<0.05 versus the value of the young rats (fixed as 1); #p<0.05 versus the amount from the same region of aged AL rats; n number of analyzed animals several reasons. Reports on variations of astrocytes density during aging are conflicting, with papers showing either increase, decrease, or no change (see Mansour et al 2008). At most, Cotrina and Nedergaard (2002) reported a 20 % increased density with aging.…”

Section: Discussionmentioning

confidence: 99%

Age- and calorie restriction-related changes in rat brain mitochondrial DNA and TFAM binding

Picca

Fracasso

Pesce

et al. 2012

AGE

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Aging markedly affects mitochondrial biogenesis and functions particularly in tissues highly dependent on the organelle's bioenergetics capability such as the brain's frontal cortex. Calorie restriction (CR) diet is, so far, the only intervention able to delay or prevent the onset of several age-related alterations in different organisms. We determined the contents of mitochondrial transcription factor A (TFAM), mitochondrial DNA (mtDNA), and the 4.8-kb mtDNA deletion in the frontal cortex from young (6-monthold) and aged (26-month-old), ad libitum-fed (AL) and calorie-restricted (CR), rats. We found a 70 % increase in TFAM amount, a 25 % loss in mtDNA content, and a 35 % increase in the 4.8-kb deletion content in the aged AL animals with respect to the young rats. TFAM-specific binding to six mtDNA regions was analyzed by mtDNA immunoprecipitation and semiquantitative polymerase chain reaction (PCR), showing a marked age-related decrease. Quantitative realtime PCR at two subregions involved in mtDNA replication demonstrated, in aged AL rats, a remarkable decrease (60-70 %) of TFAM-bound mtDNA. The decreased TFAM binding is a novel finding that may explain the mtDNA loss in spite of the compensatory TFAM increased amount. In aged CR rats, TFAM amount increased and mtDNA content decreased with respect to young rats' values, but the extent of the changes was smaller than in aged AL rats. Attenuation of the age-related effects due to the diet in the CR animals was further evidenced by the unchanged content of the 4.8-kb deletion with respect to that of young animals and by the partial prevention of the age-related decrease in TFAM binding to mtDNA.

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Aging‐related changes in astrocytes in the rat retina: imbalance between cell proliferation and cell death reduces astrocyte availability

Cited by 66 publications

References 88 publications

Progressive Retinal Degeneration in Transgenic Mice with Overexpression of Endothelin-1 in Vascular Endothelial Cells

Progressive Retinal Degeneration in Transgenic Mice with Overexpression of Endothelin-1 in Vascular Endothelial Cells

Astrocytes in Alzheimer's Disease

Age- and calorie restriction-related changes in rat brain mitochondrial DNA and TFAM binding

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