Journal: Frontiers in Cellular Neuroscience

Article Title: Transient ischemic stroke triggers sustained damage of the choroid plexus blood-CSF barrier

doi: 10.3389/fncel.2023.1279385

Figure Lengend Snippet: Dynamic changes of SPAK-NKCC1 complex phosphorylation in LVCP after ischemic stroke. (A) Representative confocal immunofluorescence staining images of phosphorylated SPAK and NKCC1 proteins in LVCP (IL: ipsilateral) at 5-day post-stroke or sham surgery. Arrow: high expression. Arrowhead: low expression. (B) Quantification of pSPAK and pNKCC1 fluorescence intensity. Data are mean ± SEM, n = 3. ** p < 0.01; *** p < 0.001.

Article Snippet: Rabbit anti-SPAK/OSR1 (Cat# 2281S) and rabbit anti-NKCC1 antibody (Cat# 85403T) were purchased from Cell Signaling.

Techniques: Phospho-proteomics, Immunofluorescence, Staining, Expressing, Fluorescence

Journal: Frontiers in Cellular Neuroscience

Article Title: Transient ischemic stroke triggers sustained damage of the choroid plexus blood-CSF barrier

doi: 10.3389/fncel.2023.1279385

Figure Lengend Snippet: Dynamic changes of SPAK-NKCC1 complex expression in ChP after ischemic stroke. (A) Representative confocal immunofluorescence staining images of SPAK and NKCC1 protein in the LVCP (IL: ipsilateral) at 1-, 5-, or 7-day post-stroke or sham surgery. Arrow: high expression. Arrowhead: low expression. (B) Quantification for fluorescence intensity of apical SPAK and NKCC1 protein in ROI. Data are mean ± SEM, n = 3–6. * p < 0.05.

Article Snippet: Rabbit anti-SPAK/OSR1 (Cat# 2281S) and rabbit anti-NKCC1 antibody (Cat# 85403T) were purchased from Cell Signaling.

Techniques: Expressing, Immunofluorescence, Staining, Fluorescence

Journal: Frontiers in Cellular Neuroscience

Article Title: Transient ischemic stroke triggers sustained damage of the choroid plexus blood-CSF barrier

doi: 10.3389/fncel.2023.1279385

Figure Lengend Snippet: Schematic illustration of ischemic stroke-induced changes of the ChP blood-CSF barrier integrity. Ischemic stroke triggers the damage of blood-CSF barrier and results in permeability increase which lasts at least 7 days post-stroke, which reflected by uptake of the albumin by CPECs, the breakdown of TJs and infiltration of circulating immune cells, etc. Ischemic stroke also causes upregulation of proinflammatory Lcn2 gene and LCN2 protein expression especially in the early acute post-stroke stage, accompanied with sustained reduction of choroidal SPAK-NKCC1 protein expression but activation of SPAK as well as NKCC1 phosphorylation. Ischemic stroke also induced infiltration of CD45 + /CD11b + myeloid cells into the ChP. Taken together, stroke-mediated damages of the ChP may lead to inflammation and dysregulation of CSF.

Article Snippet: Rabbit anti-SPAK/OSR1 (Cat# 2281S) and rabbit anti-NKCC1 antibody (Cat# 85403T) were purchased from Cell Signaling.

Techniques: Permeability, Expressing, Activation Assay, Phospho-proteomics