Modulation of apolipoprotein D and apolipoprotein E expression in rat hippocampus after entorhinal cortex lesion

Terrisse, Laurence; Séguin, Diane; Bertrand, Philìppe; Poirier, Judes; Milne, Ross W.; Rassart, Éric

doi:10.1016/s0169-328x(99)00123-0

Cited by 64 publications

(57 citation statements)

References 57 publications

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“…Studies have also supported a neuroprotective role for apoD in the nervous system. A 42% increase in apoD mRNA levels and up to 16-fold increases in protein expression have been observed in the hippocampus after entorhinal cortex lesioning (40), which results in reactive synaptogenesis and compensatory glial functions. And after peripheral nerve injury, apoD was found to be up-regulated in sites undergoing regeneration (12).…”

Section: Discussionmentioning

confidence: 98%

Increased CNS levels of apolipoprotein D in schizophrenic and bipolar subjects: Implications for the pathophysiology of psychiatric disorders

Thomas

Dean

Pavey

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

119

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Chronic administration of the atypical antipsychotic drug, clozapine, to rodents has been shown to increase the concentration of apolipoprotein D (apoD) in several area of the brain, suggesting that apoD could be involved in the therapeutic effects of antipsychotic drugs and͞or the pathology of psychotic illnesses. Here, we measured a significant decrease in the concentration of apoD in serum samples from schizophrenic patients. In contrast, apoD levels were significantly increased (92-287%) in dorsolateral prefrontal cortex (Brodmann's area 9) of schizophrenic and bipolar subjects. Elevated levels of apoD expression were also observed in the caudate of schizophrenic and bipolar subjects (68 -89%). No differences in apoD immunoreactivity were detected in occipital cortex (Brodmann's area 18) in either group, or in the hippocampus, substantia nigra, or cerebellum of the schizophrenic group. The low serum concentrations of apoD observed in these patients supports recent hypotheses involving systemic insufficiencies in lipid metabolism͞signaling in schizophrenia. Elevation of apoD expression selectively within central nervous system regions implicated in the pathology of these neuropsychiatric disorders suggests a focal compensatory response that neuroleptic drug regimens may augment.

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Section: Discussionmentioning

confidence: 98%

Increased CNS levels of apolipoprotein D in schizophrenic and bipolar subjects: Implications for the pathophysiology of psychiatric disorders

Thomas

Dean

Pavey

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

119

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“…Conversely, ApoE is expressed by glia and known to down-regulate CNS pro-inflammatory genes (Lynch et al, 2001 properties (Terrisse et al, 1999). However, ApoE expression levels are similar in the PQ-challenged WT and ApoD-KO primary cultures (not shown), as well as in the mesencephalon of mice exposed to chronic PQ treatment (see above).…”

Section: Apod Role In the Astroglial Response Tomentioning

confidence: 92%

Apolipoprotein D mediates autocrine protection of astrocytes and controls their reactivity level, contributing to the functional maintenance of paraquat-challenged dopaminergic systems

Bajo‐Grañeras¹,

Ganfornina²,

Martín-Tejedor³

et al. 2011

Glia

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The study of glial derived factors induced by injury and degeneration is important to understand the nervous system response to deteriorating conditions. We focus on Apolipoprotein D (ApoD), a Lipocalin expressed by glia and strongly induced upon aging, injury or neurodegeneration.Here we study ApoD function in the brain of wild type and ApoD-KO mice by combining in vivo experiments with astrocyte cultures. Locomotor performance, dopamine concentration, and gene expression levels in the substantia nigra were assayed in mice treated with paraquat (PQ). The regulation of ApoD transcription, a molecular screening of oxidative stress (OS)-related genes, cell viability and oxidation status, and the effects of adding human ApoD were tested in astrocyte cultures. We demonstrate that (1) ApoD is required for an adequate locomotor performance, modifies the gene expression profile of PQ-challenged nigrostriatal system, and contributes to its functional maintenance; (2) ApoD expression in astrocytes is controlled by the OSresponsive JNK pathway; (3) ApoD contributes to an autocrine protecting mechanism in astrocytes, avoiding peroxidated lipids accumulation and altering the PQ transcriptional response of genes involved in ROS managing and the inflammatory response to OS; (4) Addition of human ApoD to ApoD-KO astrocytes promotes survival through a mechanism accompanied by protein internalization and modulation of astroglial reactivity. Our data support that ApoD contributes to the endurance of astrocytes and decreases their reactivity level in vitro and in vivo. ApoD function as a maintenance factor for astrocytes would suffice to explain the observed protection by ApoD of OS-vulnerable dopaminergic circuits in vivo. V

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“…1C). As previous studies have suggested there may be compensatory changes between apoE and apoD in mice (Terrisse et al, 1999) and humans (Kim et al, 2009), possibly due to a partial overlap in lipid-binding functions, we also assessed apoE protein levels. ApoD deletion did not significantly alter apoE protein levels, although we did observe a trend (p = 0.06) for 14% lower apoE in the APP-PS1/DKO mice ( Fig.…”

Section: Generation Of App-ps1 Mice That Lack Apod or Express Human Amentioning

confidence: 99%

Apolipoprotein D modulates amyloid pathology in APP/PS1 Alzheimer's disease mice

Liu

Ruberu

Muñoz

et al. 2015

Neurobiology of Aging

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Apolipoprotein D (apoD) is expressed in the brain and levels are increased in affected brain regions in Alzheimer's disease (AD). The role that apoD may play in regulating AD pathology has not been addressed. Here, we crossed both apoD-null mice and Thy-1 human apoD transgenic mice with APP-PS1 amyloidogenic AD mice. Loss of apoD resulted in a nearly 2-fold increase in hippocampal amyloid plaque load, as assessed by immunohistochemical staining. Conversely, transgenic expression of neuronal apoD reduced hippocampal plaque load by approximately 35%. This latter finding was associated with a 60% decrease in amyloid β 1-40 peptide levels, and a 34% decrease in insoluble amyloid β 1-42 peptide. Assessment of β-site amyloid precursor protein cleaving enzyme-1 (BACE1) levels and proteolytic products of amyloid precursor protein and neuregulin-1 point toward a possible association of altered BACE1 activity in association with altered apoD levels. In conclusion, the current studies provide clear evidence that apoD regulates amyloid plaque pathology in a mouse model of AD. Disciplines Medicine and Health Sciences Publication DetailsLi, H., Ruberu, K., Sanz Munoz, S., Jenner, A. M., Spiro, A., Zhao, H., Rassart, E., Sanchez, D., Ganfornina, M. peptide levels, and a 34% decrease in insoluble amyloid-beta 1-42 peptide. Assessment of beta-site amyloid precursor protein cleaving enzyme-1 (BACE1) levels and proteolytic products of amyloid precursor protein and neuregulin-1 point towards a possible association of altered BACE1 activity in association with altered apoD levels. In conclusion, the current studies provide clear evidence that apoD regulates amyloid plaque pathology in a mouse model of AD.

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Modulation of apolipoprotein D and apolipoprotein E expression in rat hippocampus after entorhinal cortex lesion

Cited by 64 publications

References 57 publications

Increased CNS levels of apolipoprotein D in schizophrenic and bipolar subjects: Implications for the pathophysiology of psychiatric disorders

Increased CNS levels of apolipoprotein D in schizophrenic and bipolar subjects: Implications for the pathophysiology of psychiatric disorders

Apolipoprotein D mediates autocrine protection of astrocytes and controls their reactivity level, contributing to the functional maintenance of paraquat-challenged dopaminergic systems

Apolipoprotein D modulates amyloid pathology in APP/PS1 Alzheimer's disease mice

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