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Chronic infection of Toxoplasma gondii downregulates miR-132 expression in multiple brain regions in a sex-dependent manner

Published online by Cambridge University Press:  29 October 2014

YE LI
Affiliation:
Stanley Division of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins School of Medicine, Baltimore, Maryland 21287, USA Department of Psychiatry, Renmin Hospital, Wuhan University, Wuhan, PR China
GEETHA KANNAN
Affiliation:
Division of Neurobiology, Department of Psychiatry, Johns Hopkins School of Medicine, Baltimore, Maryland 21287, USA
MIKHAIL V. PLETNIKOV
Affiliation:
Division of Neurobiology, Department of Psychiatry, Johns Hopkins School of Medicine, Baltimore, Maryland 21287, USA
ROBERT H. YOLKEN
Affiliation:
Stanley Division of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins School of Medicine, Baltimore, Maryland 21287, USA
JIANCHUN XIAO*
Affiliation:
Stanley Division of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins School of Medicine, Baltimore, Maryland 21287, USA
*
*Corresponding author: Stanley Division of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins School of Medicine, Baltimore, Maryland 21287, USA. E-mail: jxiao4@jhmi.edu

Summary

MicroRNA-132 (miR-132) has been demonstrated to affect multiple neuronal functions and its dysregulation is linked to several neurological disorders. We previously showed that acute Toxoplasma gondii infection induces miR-132 expression both in vitro and in vivo. To investigate the impact of chronic infection on miR-132, we infected mice with T. gondii PRU strain and performed assessment 5 months later in six brain regions (cortex, hypothalamus, striatum, cerebellum, olfactory bulb and hippocampus) by qPCR. We found that while acute infection of T. gondii increases the expression of miR-132, chronic infection has the opposite effect. The effect varied amongst different regions of the brain and presented in a sex-dependent manner, with females exhibiting more susceptibility than males. MiR-132 and brain-derived neurotrophic factor (BDNF, an inducer of miR-132) were not co-varies in the brain areas of infected mice. T. gondii DNA/RNA was found in all tested brain regions and a selective tropism towards the hippocampus, based on bradyzoite density, was observed in both males and females. However, the expressions of miR-132 or BDNF were poorly reflected by the density of T. gondii in brain areas. Our findings highlight the importance of investigating the miR-132-mediated neuronal function in mice infected with T. gondii.

Type
Research Article
Copyright
Copyright © Cambridge University Press 2014 

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