Biology subjects

Szydlowska, K.

Publications and source records attributed to Szydlowska, K..

2 recordsLinked to original sources

bioRxiv2024

miR-155-5p/miR-674-3p presence in peripheral blood leukocytes and relative proportion of white blood cell types as biomarkers of asymptomatic and symptomatic phases of temporal lobe epilepsy

Epilepsy frequently develops as a result of brain insult, for example, brain injury or stroke. Currently, there are no tools allowing us to predict which trauma patients will eventually develop epilepsy. There is evidence that microRNAs levels are altered in the blood, making them attractive candidates for peripheral biomarkers of epilepsy. We analyzed white blood cell subpopulations containing miR-155-5p and miR-674-3p, in control and stimulated animals and in control and symptomatic or asymptomatic animals in the amygdala stimulation model. The first proposed early biomarker of epilepsy is the relative proportion of CD45RA+ B cells containing miR-155-5p and/or miR-674-3p. Others are increased number of CD45RA+ B cells containing either miR-155-5p or miR-155-5p and miR-674-3p together or decreased number of CD161+ NK cells not containing miR-155-5p nor miR-674-3p. Additionally, we found that the decreased number of CD4+ T cells can be used as a potential biomarker for identifying epileptic animals with symptomatic epilepsy.

neuroscience↗

bioRxiv2018

SorCS2 controls functional expression of amino acid transporter EAAT3 to protect neurons from oxidative stress and epilepsy-induced pathology

The family of VPS10P domain receptors emerges as central regulator of intracellular protein sorting in neurons with relevance for various brain pathologies. Here, we identified a unique role for the family member SorCS2 in protection of neurons from oxidative stress and from epilepsy-induced cell death. We show that SorCS2 acts as sorting receptor that targets the neuronal amino acid transporter EAAT3 to the plasma membrane to facilitate import of cysteine, required for synthesis of the reactive oxygen species scavenger glutathione. Absence of SorCS2 activity causes aberrant transport of EAAT3 to lysosome for catabolism and impairs cysteine uptake. As a consequence, SorCS2-deficient mice exhibit oxidative brain damage that coincides with enhanced neuronal cell death and increased mortality during epilepsy. Our findings highlight a protective role for SorCS2 in neuronal stress response and provide an explanation for upregulation of the receptor seen in surviving neurons of the human epileptic brain.

neuroscience↗