Fig. 6: Overexpression of A2AR modulates the expression of ion channel proteins in the choroid plexus (ChP). | Nature Communications

Fig. 6: Overexpression of A2AR modulates the expression of ion channel proteins in the choroid plexus (ChP).

From: Aberrant adenosine A2A receptor signaling in the choroid plexus drives CSF hypersecretion and ventriculomegaly in hydrocephalus

Fig. 6: Overexpression of A2AR modulates the expression of ion channel proteins in the choroid plexus (ChP).

A Volcano plot illustrating the differentially expressed genes (DEGs) identified upon A2AR overexpression (OE) in the ChP compared to the control group, based on bulk RNA-seq data (n = 5/group). False Discovery Rate (FDR) was obtained by correcting the P value of the hypothesis testing results of DEGs using the Benjamin-Hochberg method. B Heatmap displaying the top 50 DEGs. C Gene ontology (GO) annotation of the DEGs observed in the bulk RNA-seq data. D–H Validation of the bulk RNA-seq data by qPCR analysis of candidate gene expression (n = 5/group). I Representative immunoblots of ATP1A2 from ChP lysates of AAV-control vs. AAV-A2AR-OE mice (14 days after ICV-viral injection). J Quantitative analysis of ATP1A2 protein levels in (I) (n = 5/group) shows that A2AR-OE in the ChP led to a reduction in ATP1A2 protein levels. K Representative immunoblots of ATP1A2 in lysates of A2AR-OE transfected primary ChP epithelial cells 48 h after treatment with the NF-κB inhibitor (JSH-23, 10 μM) or vehicle. L Quantification of ATP1A2 protein levels in (K) (n = 5/group) showing that JSH-23 restored ATP1A2 levels in A2AR-OE transfected primary ChP epithelial cells. Unpaired two-tailed Student’s t test. ns: non-significant. Data are mean ± s.e.m. Source data are provided as a Source Data file.

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