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Inhibition of PirB Activity by TAT-PEP Improves Mouse Motor Ability and Cognitive Behavior
Ya-Jing Mi1, Hai Chen1,2, Na Guo1
1Institute of Basic and Translational Medicine, and School of Basic Medical Sciences, and Shaanxi Key Laboratory of Brain Disorders, Xi'an Medical UniversityXi'an, China.
Abstract:
Paired immunoglobulin-like receptor B (PirB), a functional receptor for myelin-associated inhibitory proteins, plays an important role in axon regeneration in injured brains. However, its role in normal brain function with age has not been previously investigated. Therefore in this study, we examined the expression level of PirB in the cerebral cortex, hippocampus and cerebellum of mice at 1 month, 3 months and 18 months of age. The results showed that the expression of PirB increased with age. We further demonstrated that overexpression of PirB inhibited neurite outgrowth in PC12 cells, and this inhibitory activity of PirB could be reversed by TAT-PEP, which is a recombinant soluble PirB ectodomain fused with TAT domain for blood-brain barrier penetration. In vivo study, intraperitoneal administration of TAT-PEP was capable of enhancing motor capacity and spatial learning and memory in mice, which appeared to be mediated through regulation of brain-derived neurotrophic factor (BDNF) secretion. Our study suggests that PirB is associated with aging and TAT-PEP may be a promising therapeutic agent for modulation of age-related motor and cognitive dysfunctions.
Insights
Paired immunoglobulin-like receptor B (PirB) expression increases with age, impacting brain function. A novel therapeutic, TAT-PEP, shows promise in reversing age-related cognitive and motor decline by regulating brain-derived neurotrophic factor (BDNF).
Area of Science:
- Neuroscience
- Aging Research
- Molecular Biology
Background:
- Paired immunoglobulin-like receptor B (PirB) is crucial for axon regeneration after brain injury.
- The role of PirB in normal brain aging remains largely unexplored.
Purpose of the Study:
- To investigate the age-dependent expression of PirB in the mouse brain.
- To evaluate the therapeutic potential of a novel PirB inhibitor, TAT-PEP, for age-related cognitive and motor deficits.
Main Methods:
- Quantitative analysis of PirB expression in different brain regions of mice at various ages (1, 3, and 18 months).
- In vitro studies using PC12 cells to assess PirB's effect on neurite outgrowth and the efficacy of TAT-PEP.
- In vivo experiments involving intraperitoneal administration of TAT-PEP to aged mice to assess behavioral outcomes and BDNF levels.
Main Results:
- PirB expression significantly increased with age in the cerebral cortex, hippocampus, and cerebellum.
- Overexpression of PirB inhibited neurite outgrowth in vitro, an effect reversed by TAT-PEP.
- TAT-PEP administration enhanced motor function and improved spatial learning and memory in aged mice, linked to increased BDNF secretion.
Conclusions:
- PirB expression is associated with the aging process in the brain.
- TAT-PEP demonstrates therapeutic potential for mitigating age-related motor and cognitive impairments, possibly via BDNF modulation.
