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The Adhesion GPCR GPR125 is specifically expressed in the choroid plexus and is upregulated following brain injury.

Pickering C, Hägglund M, Szmydynger-Chodobska J, Marques F, Palha JA, Waller L, Chodobski A, Fredriksson R, Lagerström MC, Schiöth HB - BMC Neurosci (2008)

Bottom Line: A single copy of GPR125 was found in many vertebrate genomes.Induction of inflammation by LPS did not change GPR125 expression.However, GPR125 expression was transiently increased (almost 2-fold) at 4 h after traumatic brain injury (TBI) followed by a decrease (approximately 4-fold) from 2 days onwards in the choroid plexus as well as increased expression (2-fold) in the hippocampus that was delayed until 1 day after injury.

View Article: PubMed Central - HTML - PubMed

Affiliation: Uppsala University, Department of Neuroscience, Functional Pharmacology, BMC, Box 593, SE-75124, Uppsala, Sweden. chris.pickering@neuro.uu.se

ABSTRACT

Background: GPR125 belongs to the family of Adhesion G protein-coupled receptors (GPCRs). A single copy of GPR125 was found in many vertebrate genomes. We also identified a Drosophila sequence, DmCG15744, which shares a common ancestor with the entire Group III of Adhesion GPCRs, and also contains Ig, LRR and HBD domains which were observed in mammalian GPR125.

Results: We found specific expression of GPR125 in cells of the choroid plexus using in situ hybridization and protein-specific antibodies and combined in situ/immunohistochemistry co-localization using cytokeratin, a marker specific for epithelial cells. Induction of inflammation by LPS did not change GPR125 expression. However, GPR125 expression was transiently increased (almost 2-fold) at 4 h after traumatic brain injury (TBI) followed by a decrease (approximately 4-fold) from 2 days onwards in the choroid plexus as well as increased expression (2-fold) in the hippocampus that was delayed until 1 day after injury.

Conclusion: These findings suggest that GPR125 plays a functional role in choroidal and hippocampal response to injury.

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Related in: MedlinePlus

In situ hybridization staining on free floating sections using 400 ng of digoxigenin (DIG)-labeled mouse GPR125 antisense probe (A and B) and sense probe (C) as control with the enzyme substrate BM-Purple. Sagittal section in A and coronal sections in B and C.
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Figure 3: In situ hybridization staining on free floating sections using 400 ng of digoxigenin (DIG)-labeled mouse GPR125 antisense probe (A and B) and sense probe (C) as control with the enzyme substrate BM-Purple. Sagittal section in A and coronal sections in B and C.

Mentions: For localization, in situ hybridization was performed using the visible enzyme substrate BM-Purple and 400 ng of digoxigenin-labeled GPR125 probe. The complete series of this can be seen in Additional file 3. Staining was limited to two key areas; the choroid plexus and neighbouring cerebral cortex (Figure 3A and 3B) and the piriform cortex area 2 (Additional file 3) while no staining was observed in the hippocampus. A sense probe for GPR125 did not stain these areas (data not shown).


The Adhesion GPCR GPR125 is specifically expressed in the choroid plexus and is upregulated following brain injury.

Pickering C, Hägglund M, Szmydynger-Chodobska J, Marques F, Palha JA, Waller L, Chodobski A, Fredriksson R, Lagerström MC, Schiöth HB - BMC Neurosci (2008)

In situ hybridization staining on free floating sections using 400 ng of digoxigenin (DIG)-labeled mouse GPR125 antisense probe (A and B) and sense probe (C) as control with the enzyme substrate BM-Purple. Sagittal section in A and coronal sections in B and C.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2571103&req=5

Figure 3: In situ hybridization staining on free floating sections using 400 ng of digoxigenin (DIG)-labeled mouse GPR125 antisense probe (A and B) and sense probe (C) as control with the enzyme substrate BM-Purple. Sagittal section in A and coronal sections in B and C.
Mentions: For localization, in situ hybridization was performed using the visible enzyme substrate BM-Purple and 400 ng of digoxigenin-labeled GPR125 probe. The complete series of this can be seen in Additional file 3. Staining was limited to two key areas; the choroid plexus and neighbouring cerebral cortex (Figure 3A and 3B) and the piriform cortex area 2 (Additional file 3) while no staining was observed in the hippocampus. A sense probe for GPR125 did not stain these areas (data not shown).

Bottom Line: A single copy of GPR125 was found in many vertebrate genomes.Induction of inflammation by LPS did not change GPR125 expression.However, GPR125 expression was transiently increased (almost 2-fold) at 4 h after traumatic brain injury (TBI) followed by a decrease (approximately 4-fold) from 2 days onwards in the choroid plexus as well as increased expression (2-fold) in the hippocampus that was delayed until 1 day after injury.

View Article: PubMed Central - HTML - PubMed

Affiliation: Uppsala University, Department of Neuroscience, Functional Pharmacology, BMC, Box 593, SE-75124, Uppsala, Sweden. chris.pickering@neuro.uu.se

ABSTRACT

Background: GPR125 belongs to the family of Adhesion G protein-coupled receptors (GPCRs). A single copy of GPR125 was found in many vertebrate genomes. We also identified a Drosophila sequence, DmCG15744, which shares a common ancestor with the entire Group III of Adhesion GPCRs, and also contains Ig, LRR and HBD domains which were observed in mammalian GPR125.

Results: We found specific expression of GPR125 in cells of the choroid plexus using in situ hybridization and protein-specific antibodies and combined in situ/immunohistochemistry co-localization using cytokeratin, a marker specific for epithelial cells. Induction of inflammation by LPS did not change GPR125 expression. However, GPR125 expression was transiently increased (almost 2-fold) at 4 h after traumatic brain injury (TBI) followed by a decrease (approximately 4-fold) from 2 days onwards in the choroid plexus as well as increased expression (2-fold) in the hippocampus that was delayed until 1 day after injury.

Conclusion: These findings suggest that GPR125 plays a functional role in choroidal and hippocampal response to injury.

Show MeSH
Related in: MedlinePlus