engleski

Expression of neuroplastin in the brain cortex and cerebellum of Toll-like receptor 2 knock-out mouse

The aim of this study was to investigate the expression of two isoforms of synaptic glycoprotein neuroplastin (Np), Np55 and Np65, in the brain cortex and cerebellum of mouse lacking Toll-like receptor 2 (TLR2). Since TLRs are widely expressed in mammalian brain and involved in neurodegeneration and hypoxic stress, TLR2 knock- out (KO) mouse model (B6.129-Tlr2tm1Kir/J) is especially intriguing to analyze Np expression due to following evidence: 1) there is a threefold increase in Np65 in rat forebrain following transient ischemia suggesting a role of Np65 in recovery from ischemic insult ; 2) Np contributes to neuronal energy metabolism by acting as chaperone of monocarboxylate transporter MCT2 ; 3) Np65 KO mice have been found to be more susceptible to ischemic brain lesions. In TLR2 KO mice, attenuated neurodegeneration upon hypoxic stimuli has been described due to reduced microglial activation. To fill in the gaps in biochemical description of this model we investigated expression of Np55 and Np65 isoforms in brain tissue derived from wt and TLR2 KO mice. Membrane fractions were isolated from cortical and cerebellar tissue samples dissected from 22 animals, in which expression of two Np isoforms was determined by Western blotting. Results showed statistically significant increase of both Np55 and Np65 in cortex and decrease of Np55 in cerebellum in male KO vs wt mice. Obtained data are introduction for a larger study which will address potential interplay of Np and TLR2 as well as influence of hypoxia on Np expression in different brain regions.

neuroplastin, membrane

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