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Histological localization of PUM1 in brain tissue from patients with epilepsy. ( a to f ) The expression level of CLDN-5 mRNA in resected human brain samples. The RNAs were isolated from the resected brain tissues obtained from control subjects ( n = 11) and patients with epilepsy ( n = 12). ( a ) CLDN-5, PUM1 and PUM2 mRNA expression levels between samples collected from control and epilepsy patients. CLDN-5 mRNA levels in the samples were broken down by ( b ) the difference of rs10314 genotypes (G is wild-type allele and C is rs10314 allele) and ( c ) seizure frequency. The data represents mean ± SD. ns, not significant ( p > 0.05); *p value ≤ 0.05; **p value ≤ 0.01. The correlation between CLDN-5 mRNA and ( d ) years of epilepsy, ( e ) PUM1 and ( f ) PUM2 mRNA levels. Spearman r values and P values are indicated. ( g ) Representative confocal images of human brain sections stained with anti-PUM1 antibody. A part of the hippocampal region showed a granular PUM1 staining pattern. Red; PUM1, Green; CLDN-5. Blue; nuclei. ( h ) The evaluation of the induction of stress granules in vascular endothelial cells in human brain sections (high CLDN-5). Sections were stained with anti-CLDN-5 (green) and stress granule marker, <t>anti-p-eIF-2α</t> or anti-PUM1 (red). Nuclei (blue) were counterstained with Hoechst
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Histological localization of PUM1 in brain tissue from patients with epilepsy. ( a to f ) The expression level of CLDN-5 mRNA in resected human brain samples. The RNAs were isolated from the resected brain tissues obtained from control subjects ( n = 11) and patients with epilepsy ( n = 12). ( a ) CLDN-5, PUM1 and PUM2 mRNA expression levels between samples collected from control and epilepsy patients. CLDN-5 mRNA levels in the samples were broken down by ( b ) the difference of rs10314 genotypes (G is wild-type allele and C is rs10314 allele) and ( c ) seizure frequency. The data represents mean ± SD. ns, not significant ( p > 0.05); *p value ≤ 0.05; **p value ≤ 0.01. The correlation between CLDN-5 mRNA and ( d ) years of epilepsy, ( e ) PUM1 and ( f ) PUM2 mRNA levels. Spearman r values and P values are indicated. ( g ) Representative confocal images of human brain sections stained with anti-PUM1 antibody. A part of the hippocampal region showed a granular PUM1 staining pattern. Red; PUM1, Green; CLDN-5. Blue; nuclei. ( h ) The evaluation of the induction of stress granules in vascular endothelial cells in human brain sections (high CLDN-5). Sections were stained with anti-CLDN-5 (green) and stress granule marker, <t>anti-p-eIF-2α</t> or anti-PUM1 (red). Nuclei (blue) were counterstained with Hoechst
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Image Search Results


Histological localization of PUM1 in brain tissue from patients with epilepsy. ( a to f ) The expression level of CLDN-5 mRNA in resected human brain samples. The RNAs were isolated from the resected brain tissues obtained from control subjects ( n = 11) and patients with epilepsy ( n = 12). ( a ) CLDN-5, PUM1 and PUM2 mRNA expression levels between samples collected from control and epilepsy patients. CLDN-5 mRNA levels in the samples were broken down by ( b ) the difference of rs10314 genotypes (G is wild-type allele and C is rs10314 allele) and ( c ) seizure frequency. The data represents mean ± SD. ns, not significant ( p > 0.05); *p value ≤ 0.05; **p value ≤ 0.01. The correlation between CLDN-5 mRNA and ( d ) years of epilepsy, ( e ) PUM1 and ( f ) PUM2 mRNA levels. Spearman r values and P values are indicated. ( g ) Representative confocal images of human brain sections stained with anti-PUM1 antibody. A part of the hippocampal region showed a granular PUM1 staining pattern. Red; PUM1, Green; CLDN-5. Blue; nuclei. ( h ) The evaluation of the induction of stress granules in vascular endothelial cells in human brain sections (high CLDN-5). Sections were stained with anti-CLDN-5 (green) and stress granule marker, anti-p-eIF-2α or anti-PUM1 (red). Nuclei (blue) were counterstained with Hoechst

Journal: Fluids and Barriers of the CNS

Article Title: Pumilio-1 mediated translational control of claudin-5 at the blood-brain barrier

doi: 10.1186/s12987-024-00553-5

Figure Lengend Snippet: Histological localization of PUM1 in brain tissue from patients with epilepsy. ( a to f ) The expression level of CLDN-5 mRNA in resected human brain samples. The RNAs were isolated from the resected brain tissues obtained from control subjects ( n = 11) and patients with epilepsy ( n = 12). ( a ) CLDN-5, PUM1 and PUM2 mRNA expression levels between samples collected from control and epilepsy patients. CLDN-5 mRNA levels in the samples were broken down by ( b ) the difference of rs10314 genotypes (G is wild-type allele and C is rs10314 allele) and ( c ) seizure frequency. The data represents mean ± SD. ns, not significant ( p > 0.05); *p value ≤ 0.05; **p value ≤ 0.01. The correlation between CLDN-5 mRNA and ( d ) years of epilepsy, ( e ) PUM1 and ( f ) PUM2 mRNA levels. Spearman r values and P values are indicated. ( g ) Representative confocal images of human brain sections stained with anti-PUM1 antibody. A part of the hippocampal region showed a granular PUM1 staining pattern. Red; PUM1, Green; CLDN-5. Blue; nuclei. ( h ) The evaluation of the induction of stress granules in vascular endothelial cells in human brain sections (high CLDN-5). Sections were stained with anti-CLDN-5 (green) and stress granule marker, anti-p-eIF-2α or anti-PUM1 (red). Nuclei (blue) were counterstained with Hoechst

Article Snippet: The sections were incubated with mouse anti-CLDN-5 antibodies (clone 4C3C2, Thermo Fisher Scientific) and rabbit anti-PUM1 antibodies (clone EPR3795, Abcam) or rabbit anti- p-eIF-2α antibodies (44-728G, Thermo Fisher Scientific) in 1% NGS overnight at 4 °C.

Techniques: Expressing, Isolation, Staining, Marker

Celecoxib inhibited the excessive activation of ER stress during diabetes-induced muscle atrophy. (A) Western blotting results of p-Perk, p-EIF-2α, ATF4 and Chop. (B–E) The grayscale value statistics of p-Perk, p-EIF-2α, ATF4 and Chop. Data are presented as mean ± SD, n ≥ 3; **, p < 0.01 DM versus control; ***, p < 0.001 DM versus control; ##, p < 0.01 DM + CXB versus DM; ###, p < 0.001 DM + CXB versus DM. DM: diabetes mellitus; CXB: celecoxib.

Journal: Frontiers in Pharmacology

Article Title: Celecoxib ameliorates diabetic sarcopenia by inhibiting inflammation, stress response, mitochondrial dysfunction, and subsequent activation of the protein degradation systems

doi: 10.3389/fphar.2024.1344276

Figure Lengend Snippet: Celecoxib inhibited the excessive activation of ER stress during diabetes-induced muscle atrophy. (A) Western blotting results of p-Perk, p-EIF-2α, ATF4 and Chop. (B–E) The grayscale value statistics of p-Perk, p-EIF-2α, ATF4 and Chop. Data are presented as mean ± SD, n ≥ 3; **, p < 0.01 DM versus control; ***, p < 0.001 DM versus control; ##, p < 0.01 DM + CXB versus DM; ###, p < 0.001 DM + CXB versus DM. DM: diabetes mellitus; CXB: celecoxib.

Article Snippet: The antibodies included: β-Tubulin (#ab6046), Cox2 (#ab15191), IL-1β(#ab254360), Nox2(#ab129068), Nox4(#ab109225), GPX1(#ab22604), Nrf2(#ab137550), Fbx32(#ab168372), MHC(#ab91506), Beclin1(#ab207612), ATG7(#ab133528), PGC1α(#ab191838), IL-6 (#ab9731), Sirt1 (#ab110304), BNIP3 (#ab10433), Goat Anti-Rabbit IgG H&L (HRP) (#ab205718), Goat Anti-Mouse IgG H&L (HRP) (#ab205719) from Abcam; CD68 (#38005), MuRF1 (#38580) from SAB; CD86 (#26903-1-AP), PTGES2 (#10881-1-AP), TNF-α (#60291-1-lg) from Proteintech; p-NF-κB (#3033S), p-Stat3 (Tyr705, #9145S), NLRP3(#30835S), Caspase1 (E9R2D, #83383S), Perk (#3192S), EIF-2α (#9722S), p-EIF-2α (#9721S), ATF-4 (#11815S), Chop (#2895S), Foxo3a (#12829S) from Cell Signaling Technology; p-Perk (#PA5-40294) from Invitrogen; LC3II (#M186-3) from MBL.

Techniques: Activation Assay, Western Blot, Control