Overexpression of Brain- and Glial Cell Line-Derived Neurotrophic Factors Is Neuroprotective in an Animal Model of Acute Hypobaric Hypoxia.
Maria S GavrishMark D UrazovTatiana A MishchenkoVictoria D TurubanovaEkaterina A EpifanovaVictoria G Krut'Alexey A BabaevMaria V VedunovaElena V MitroshinaPublished in: International journal of molecular sciences (2022)
Currently, the role of the neurotrophic factors BDNF and GDNF in maintaining the brain's resistance to the damaging effects of hypoxia and functional recovery of neural networks after exposure to damaging factors are actively studied. The assessment of the effect of an increase in the level of these neurotrophic factors in brain tissues using genetic engineering methods on the resistance of laboratory animals to hypoxia may pave the way for the future clinical use of neurotrophic factors BDNF and GDNF in the treatment of hypoxic damage. This study aimed to evaluate the antihypoxic and neuroprotective properties of BDNF and GDNF expression level increase using adeno-associated viral vectors in modeling hypoxia in vivo. To achieve overexpression of neurotrophic factors in the central nervous system's cells, viral constructs were injected into the brain ventricles of newborn male C57Bl6 (P0) mice. Acute hypobaric hypoxia was modeled on the 30th day after the injection of viral vectors. Survival, cognitive, and mnestic functions in the late post-hypoxic period were tested. Evaluation of growth and weight characteristics and the neurological status of animals showed that the overexpression of neurotrophic factors does not affect the development of mice. It was found that the use of adeno-associated viral vectors increased the survival rate of male mice under hypoxic conditions. The present study indicates that the neurotrophic factors' overexpression, induced by the specially developed viral constructs carrying the BDNF and GDNF genes, is a prospective neuroprotection method, increasing the survival rate of animals after hypoxic injury.
Keyphrases
- sars cov
- cerebral ischemia
- cell proliferation
- endothelial cells
- transcription factor
- white matter
- resting state
- type diabetes
- body mass index
- cell death
- adipose tissue
- physical activity
- spinal cord injury
- neural network
- insulin resistance
- skeletal muscle
- drug induced
- intensive care unit
- functional connectivity
- dna methylation
- ultrasound guided
- blood brain barrier
- metabolic syndrome
- cell cycle arrest
- combination therapy