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SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs

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Abcb1a and Abcb1b expression in senescence-accelerated mouse (SAM).

Bin Wu¹, Masaki Ueno, Takashi Kusaka

¹Department of Pathology and Host Defense, Faculty of Medicine, Kagawa University, Kagawa 761-0793, Japan.

Neuroscience Letters

|May 12, 2009

Summary

Senescence-accelerated mouse (SAM)R1 mice with an Abcb1a gene mutation show decreased P-glycoprotein expression in the brain compared to SAM P8 mice. This difference highlights SAM strains as valuable tools for studying brain drug delivery transporters.

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Induction and Validation of Cellular Senescence in Primary Human Cells

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Published on: June 20, 2018

Area of Science:

Neuroscience
Pharmacology
Genetics

Background:

Senescence-accelerated mouse (SAM) strains exhibit genetic variations, with SAMR1 possessing a spontaneous retroviral insertional mutation in the ATP-binding cassette, sub-family B, member 1A (Abcb1a) gene, unlike SAMP8.
P-glycoprotein, encoded by the Abcb1 gene, is a key efflux transporter in the cerebral vasculature, influencing drug delivery to the brain.

Purpose of the Study:

To investigate the differential gene and protein expression of ATP-binding cassette transporters, specifically Abcb1a, Abcb1b, Abcc, and Abcg2, and P-glycoprotein in the brains of SAMR1 (mutant) and SAMP8 (wild-type) mice.
To evaluate the impact of the Abcb1a mutation on P-glycoprotein expression and its potential role in brain drug delivery.

Main Methods:

Real-time quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) was employed to assess gene expression levels.
Western blotting and immunohistochemical techniques were utilized for protein expression analysis of P-glycoprotein.
Brain samples from SAMR1 and SAMP8 mice were analyzed.

Main Results:

SAMR1 mice exhibited significantly decreased Abcb1a gene expression and P-glycoprotein protein levels compared to SAMP8 mice.
Conversely, Abcb1b gene expression was found to be increased in SAMR1 mice relative to SAMP8 mice.
No significant differences in Abcc and Abcg2 gene expression were observed between the two strains. P-glycoprotein immunolocalization was consistent in brain vasculature, including endothelial and astrocytic cells.

Conclusions:

The Abcb1a gene mutation in SAMR1 mice leads to reduced Abcb1a expression and P-glycoprotein levels, despite increased Abcb1b expression.
The findings suggest that the Abcb1b gene upregulation does not compensate for the decreased P-glycoprotein expression in SAMR1 mice.
The distinct transporter profiles of SAMR1 and SAMP8 mice offer a valuable model for investigating the roles of Abcb1a and Abcb1b in brain drug delivery.