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Age-related changes in P-glycoprotein expression in senescence-accelerated mouse
Bin Wu1, Masaki Ueno, Masayuki Onodera
1Department of Pathology and Host Defense, Faculty of Medicine, Kagawa University, Kagawa 761-0793, Japan.
Current Aging Science
|December 22, 2009
Summary
Aging increases P-glycoprotein and Abcb1 gene expression in senescence-accelerated mice (SAMP8), suggesting a protective response against toxic substances in the brain. This contrasts with control mice (SAMR1), indicating age-related changes in blood-brain barrier transporters.
Area of Science:
- Neuroscience
- Molecular Biology
- Gerontology
Background:
- P-glycoprotein (encoded by ATP-binding cassette, sub-family B [Abcb1]) is a key efflux transporter in cerebral vessels.
- Age-related blood-brain barrier (BBB) damage is observed in senescence-accelerated mice (SAMP8), impacting cognitive functions.
Purpose of the Study:
- To investigate age-related changes in P-glycoprotein and Abcb1 gene expression in the brains of SAMP8 mice.
- To compare these changes with those in SAMR1 mice, which have an Abcb1a gene mutation.
Main Methods:
- Real-time quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) for gene expression.
- Western blotting and immunohistochemistry for protein expression analysis.
- Comparison between SAMP8 and SAMR1 mouse models.
Main Results:
- P-glycoprotein and Abcb1a/b gene expression increased with aging in SAMP8 mice.
- SAMR1 mice showed decreased P-glycoprotein and Abcb1a expression but increased Abcb1b expression compared to SAMP8.
- P-glycoprotein was localized in endothelial cells and astrocytes within vessel walls.
Conclusions:
- Aging in SAMP8 mice is associated with increased expression of Abcb1 genes and P-glycoprotein.
- These findings suggest an age-related compensatory mechanism to protect the brain from toxic substances.
- Abcb1a gene mutation in SAMR1 mice influences transporter expression patterns.