Disease relevance of Apod

• Increased expression of apolipoprotein D following experimental traumatic brain injury [1].

High impact information on Apod

• Regeneration-associated high level expression of apolipoprotein D mRNA in endoneurial fibroblasts of peripheral nerve [2].
• A cDNA clone containing the entire coding region of rat apolipoprotein D (Apo D) was isolated from a cDNA library of regenerating sciatic nerve by differential hybridization [2].
• Apo D protein (Mr 32.8 kd) was secreted and accumulated in the endoneurial extracellular space where it could be detected in lipoprotein fractions by immunoblotting using established antibodies to human Apo D [2].
• Using transverse sections and primary cell cultures from regenerating nerve, Apo D transcripts could be localized by in situ hybridization in endoneurial fibroblasts but not in Schwann cells, macrophages or perineurial and epineurial cells [2].
• Four gene clusters displayed a progressive increase in expression over time and included 50 genes linked to cell motility, lipid synthesis and trafficking (i.e. ApoD, NPC1, G3P-dehydrogenase1, and Choline kinase) or cell death-regulating genes such as mitochondrial CLIC [3].

Biological context of Apod

• Identification, characterization, and tissue distribution of apolipoprotein D in the rat [4].
• One gene codes for apolipoprotein D, which is thought to be involved in lipid metabolism [5].
• Apolipoprotein D immunoreactivity peaked by day 3, coincident with neuronal cell death, and declined thereafter, reaching very low levels by day 7 [6].
• Apolipoprotein D gene expression in the rat brain and light and electron microscopic immunocytochemistry of apolipoprotein D expression in the cerebellum of neonatal, immature and adult rats [7].
• Apolipoprotein D gene expression was first observed in embryonic day 12 rat brain, with a moderate increase in apolipoprotein D messenger RNA levels towards the later part (embryonic days 15-17) of gestation [7].

Anatomical context of Apod

• Expression of apolipoprotein D, a member of the lipocalin superfamily of transporter proteins, was investigated in the kainic acid-lesioned rat hippocampus [6].
• Oligodendrocytes in the cerebella of two-week-old animals were strongly apolipoprotein D positive, with immunoreactivity declining in older animals [7].
• In contrast to the neuronal expression of apolipoprotein D, apolipoprotein E immunoreactivity was observed predominantly in degenerating astrocytes [6].
• Besides pyramidal neurons, apolipoprotein D immunoreactivity was also observed in a small number of reactive glial cells in the affected CA fields, but not in the vascular compartments at any time-point [6].

Associations of Apod with chemical compounds

• Apolipoprotein-D (apoD), a member of the lipocalin family of proteins, binds to arachidonic acid and cholesterol among other hydrophobic molecules [8].
• By contrast, kainic acid-injected rats showed apolipoprotein D immunoreactivity in the pyramidal neurons of the affected CA fields 24-48 h after injection of the excitotoxin, at a time when there was no histological evidence of cell death [6].
• Using an anti-rat apolipoprotein D antibody and biotin avidin-enhanced immunocytochemistry, in the normal rat hippocampus there was little apolipoprotein D expression, that was restricted mainly to scattered astrocytes [6].

Other interactions of Apod

• Genes whose expression levels were found to be most altered included preprolactin (downregulated) and mitogen-activated protein kinase (MAP kinase 1; upregulated) in the hippocampus, and acyl-CoA synthetase (downregulated) and apolipoprotein D (upregulated) in the striatum [9].

Analytical, diagnostic and therapeutic context of Apod

• Moderately increased levels of Apo D transcripts were found in transected nerves, which were prevented from regeneration by ligation [2].

References