Apolipoprotein D—An atypical apolipoprotein

Weech, Philip K.; Provost, Pierre R.; Tremblay, Nathalie; Camato, R; Milne, Ross W.; Marcel, Yves L.; Rassart, Éric

doi:10.1016/0163-7827(91)90023-x

Cited by 41 publications

(29 citation statements)

References 33 publications

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“…ApoD, originally identified as a component of plasma high‐density lipoproteins (HDL) (McConathy and Alaupovic 1973), is an atypical apolipoprotein in that it does not share sequence homology with other apolipoproteins (Weech et al . 1991), but rather, it is a member of the lipocalin superfamily of proteins, which function in the transport of small hydrophobic molecules (Flower 1994).…”

Section: Discussionmentioning

confidence: 99%

Clozapine increases apolipoprotein D expression in rodent brain: towards a mechanism for neuroleptic pharmacotherapy

Thomas

Danielson

Nelson

et al. 2001

Journal of Neurochemistry

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In contrast to typical neuroleptic drugs, which have high affinities for dopamine D2 receptors, clozapine binds to multiple neurotransmitter receptors. The mechanisms responsible for its superior clinical efficacy over typical neuroleptics remain unknown. Using an automated genomics approach, total gene expression analysis (TOGA), we found an approximately threefold increase in the accumulation of the mRNA encoding apolipoprotein D (apoD) in mouse striatum in response to chronic treatment with clozapine. While in control animals, apoD is expressed predominantly in astrocytes, in situ hybridization and immunohistochemical studies indicated a substantial increase in apoD expression in neurons of the striatum, globus pallidus and thalamus after 2 weeks of clozapine treatment. Clozapine-induced increases in apoD expression were also observed in some white matter regions. These results suggest that apoD is a mediator in the mechanisms of clozapine and thus that deficiencies in aspects of lipid metabolism may be responsible for psychoses.

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Section: Discussionmentioning

confidence: 99%

Clozapine increases apolipoprotein D expression in rodent brain: towards a mechanism for neuroleptic pharmacotherapy

Thomas

Danielson

Nelson

et al. 2001

Journal of Neurochemistry

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“…These results should be integrated in the comprehension of E 2 action in Lpl regulation. Moreover, in the ER␣KO mice, E 2 downregulated apolipoprotein D (Apod) whose protein plays an important role in the homeostasis and housekeeping, by transporting a hydrophobic ligand [43]. Zhou et al [44] have demonstrated that the E 2 has no effect on Apod while E 2 /androgen suppresses it via androgen effect on ER␣.…”

Section: Energy Metabolismmentioning

confidence: 98%

Regulation of gene expression by estrogen in mammary gland of wild type and estrogen receptor alpha knockout mice

Aboghe

Yoshioka

Phaneuf

et al. 2009

The Journal of Steroid Biochemistry and Molecular Biology

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“…Moreover, the ApoD amino acid sequence does not show any similarity to that of any other apolipoproteins (except for ApoM, which is a member of the outlier lipocalin subfamily), but within mammals, it has the highest degree of homology to the retinol binding protein, RBP4. In view of these peculiarities, ApoD has been termed an atypical apolipoprotein (Weech et al., 1991). …”

Section: Apodmentioning

confidence: 99%

Apolipoprotein D takes center stage in the stress response of the aging and degenerative brain

Dassati

Waldner

Schweigreiter

2014

Neurobiology of Aging

125

109

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Apolipoprotein D (ApoD) is an ancient member of the lipocalin family with a high degree of sequence conservation from insects to mammals. It is not structurally related to other major apolipoproteins and has been known as a small, soluble carrier protein of lipophilic molecules that is mostly expressed in neurons and glial cells within the central and peripheral nervous system. Recent data indicate that ApoD not only supplies cells with lipophilic molecules, but also controls the fate of these ligands by modulating their stability and oxidation status. Of particular interest is the binding of ApoD to arachidonic acid and its derivatives, which play a central role in healthy brain function. ApoD has been shown to act as a catalyst in the reduction of peroxidized eicosanoids and to attenuate lipid peroxidation in the brain. Manipulating its expression level in fruit flies and mice has demonstrated that ApoD has a favorable effect on both stress resistance and life span. The APOD gene is the gene that is upregulated the most in the aging human brain. Furthermore, ApoD levels in the nervous system are elevated in a large number of neurologic disorders including Alzheimer's disease, schizophrenia, and stroke. There is increasing evidence for a prominent neuroprotective role of ApoD because of its antioxidant and anti-inflammatory activity. ApoD emerges as an evolutionarily conserved anti-stress protein that is induced by oxidative stress and inflammation and may prove to be an effective therapeutic agent against a variety of neuropathologies, and even against aging.

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Apolipoprotein D—An atypical apolipoprotein

Cited by 41 publications

References 33 publications

Clozapine increases apolipoprotein D expression in rodent brain: towards a mechanism for neuroleptic pharmacotherapy

Clozapine increases apolipoprotein D expression in rodent brain: towards a mechanism for neuroleptic pharmacotherapy

Regulation of gene expression by estrogen in mammary gland of wild type and estrogen receptor alpha knockout mice

Apolipoprotein D takes center stage in the stress response of the aging and degenerative brain

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