Additional file 1 of Recombinant Slit2 suppresses neuroinflammation and Cdc42-mediated brain infiltration of peripheral immune cells via Robo1–srGAP1 pathway in a rat model of germinal matrix hemorrhage

Additional file 1: Figure S1. Cellular locations of Slit2 and Robo1 in brain at 5 days after GMH. Representative microphotograph of immunofluorescence staining showed a co-localization of Slit2 (A) or Robo1 (B) with neuron (NeuN) and astrocyte (GFAP) across the brain section, respectively. Co-localization of Robo1 (B) with CD68-positive macrophage or MPO positive neutrophil was presented at the peri-lesion brain area. “*” symbol indicates the location of lesion Scale bar=100 μm. Figure S2. Effects of recombinant Slit2 on neuronal death in brain at 1 days after GMH. TUNEL staining showed the aggravated degree of DNA breakage (A) after GMH, which were reduced by rSlit2 treatment. “*” symbol indicates the location of lesion. Scale bar=100μm. Western blotting image and quantitative analysis showed that brain cleaved caspase-3 (B) expressions increased after GMH, which were reduced by rSlit2 treatment. N=6/group. Mean±SEM. ANOVA, Tukey. *P<0.05 vs. Sham, #P<0.05 vs. GMH+Vehicle. Figure S3. Effects of recombinant Slit2 on peripheral immune cells infiltration into brain at 1 and 5 days after GMH. MPO immunofluorescence staining showed that MPO positive neutrophils were concentrated in the peri-lesion area at day 1(A) and day 5(B) after GMH, and  the number of MPO positive neutrophils were reduced by rSlit2 treatment. The lesion was located in the upper or/and left. Scale bar=100μm

Additional file 1 of Aprepitant attenuates NLRC4-dependent neuronal pyroptosis via NK1R/PKCδ pathway in a mouse model of intracerebral hemorrhage

Additional file 1. Changes in protein expression of NK1R in the hippocampal region after ICH

Additional file 3 of Activation of Frizzled-7 attenuates blood–brain barrier disruption through Dvl/β-catenin/WISP1 signaling pathway after intracerebral hemorrhage in mice

Additional file 3: Figure S3. Effects of WISP1 CRISPR (activation or KO) on BBB permeability. Evans blue extravasation at 72 h (A, B) after ICH. The bars represent the mean ± SD. ICH = intracerebral hemorrhage; WISP1 = WNT1-inducible signaling pathway protein 1; ACT Ctrl = activation control; KO Ctrl = knockdown control; WISP1 ACT = activation of WISP1; WISP1 KO = knockdown of WISP1. n = 4 per group. *p < 0.05 vs. sham group; #p < 0.05 vs. ICH + ACT Ctrl group; &p < 0.05 vs. ICH + KO Ctrl group; @p < 0.05 vs. ICH + WISP1 KO group; One-way ANOVA, Tukey’s post hoc test

Table_1_Human Galectin-7 Gene LGALS7 Promoter Sequence Polymorphisms and Risk of Spontaneous Intracerebral Hemorrhage: A Prospective Study.docx

Background and purposeDespite evidence for the role of genetic factors in stroke, only a small proportion of strokes have been clearly attributed to monogenic factors, due to phenotypic heterogeneity. The goal of this study was to determine whether a significant relationship exists between human galectin-7 gene LGALS7 promoter region polymorphisms and the risk of stroke due to non-traumatic intracerebral hemorrhage (ICH).MethodsThis two-stage genetic association study included an initial exploratory stage followed by a discovery stage. During the exploratory stage, transgenic galectin-7 mice or transgenic mice with the scrambled sequence of the hairpin structure –silenced down gene LGALS7—were generated and then expressed differentially expressed proteins and galectin-7-interacting proteins were identified through proteomic analysis. During the discovery stage, a single-nucleotide polymorphism (SNP) genotyping approach was used to determine associations between 2 LGALS7 SNPs and ICH stroke risk for a cohort of 24 patients with stroke of the Chinese Han population and 70 controls.ResultsDuring the exploratory phase, LGALS7 expression was found to be decreased in TGLGALS–DOWN mice as compared to its expression in TGLGALS mice. During the discovery phase, analysis of LGALS7 sequences of 24 non-traumatic ICH cases and 70 controls led to the identification of 2 ICH susceptibility loci: a genomic region on 19q13.2 containing two LGALS7 SNPs, rs567785577 and rs138945880, whereby the A allele of rs567785577 and the T allele of rs138945880 were associated with greater risk of contracting ICH [for T and A vs. C and G, unadjusted odds ratio (OR) = 13.5; 95% CI = 2.249–146.5; p = 0.002]. This is the first study to genotype the galectin-7 promoter in patients with hemorrhagic stroke. Genotype and allele association tests and preliminary analysis of patients with stroke revealed that a single locus may be a genetic risk factor for hemorrhagic stroke.ConclusionA and T alleles of two novel SNP loci of 19q13.2, rs567785577 and rs138945880, respectively, were evaluated for associations with susceptibility to ICH. Further studies with expanded case numbers that include subjects of other ethnic populations are needed to elucidate mechanisms underlying associations between these SNPs and ICH risk.</p

Additional file 1 of Activation of Frizzled-7 attenuates blood–brain barrier disruption through Dvl/β-catenin/WISP1 signaling pathway after intracerebral hemorrhage in mice

Additional file 1: Figure S1. Efficacy of FZD7 CRISPR activation or knockdown in naive and ICH mice. (A) Representative western blot bands at 24 h after ICH. (B-C) Densitometric quantification of FZD7. n = 4 per group; Ctrl CRISPR = control CRISPR; CRISPR ACT = Frizzled-7 CRISPR activation; CRISPR KO = Frizzled-7 CRISPR KO. Data was represented as mean ± SD. FZD7 = Frizzled-7; ICH = intracerebral hemorrhage. *p < 0.05 vs. Naive + Control CRISPR, @p < 0.05 vs. ICH + Control CRISPR; One-way ANOVA, Tukey’s post hoc test

Additional file 2 of Activation of Frizzled-7 attenuates blood–brain barrier disruption through Dvl/β-catenin/WISP1 signaling pathway after intracerebral hemorrhage in mice

Additional file 2: Figure S2. Efficacy of WISP1 CRISPR activation or knockdown in naive and ICH mice. (A) Representative western blot bands at 24 h after ICH. (B-C) Densitometric quantification of WISP1. n = 4 per group; Ctrl CRISPR = control CRISPR; CRISPR ACT = WISP1 CRISPR activation; CRISPR KO = WISP1 CRISPR KO. Data was represented as mean ± SD. ICH = intracerebral hemorrhage, WISP1 = WNT1-inducible signaling pathway protein 1. *p < 0.05 vs. Naive + Control CRISPR, @p < 0.05 vs. ICH + Control CRISPR; One-way ANOVA, Tukey’s post hoc test

Additional file 4 of Inhibition of lysophosphatidic acid receptor 1 relieves PMN recruitment in CNS via LPA1/TSP1/CXCR2 pathway and alleviates disruption on blood-brain barrier following intracerebral haemorrhage in mice

Supplementary Material

Additional file 3 of Inhibition of lysophosphatidic acid receptor 1 relieves PMN recruitment in CNS via LPA1/TSP1/CXCR2 pathway and alleviates disruption on blood-brain barrier following intracerebral haemorrhage in mice

Supplementary Material

Additional file 2 of Inhibition of lysophosphatidic acid receptor 1 relieves PMN recruitment in CNS via LPA1/TSP1/CXCR2 pathway and alleviates disruption on blood-brain barrier following intracerebral haemorrhage in mice

Supplementary Material

Additional file 1 of Inhibition of lysophosphatidic acid receptor 1 relieves PMN recruitment in CNS via LPA1/TSP1/CXCR2 pathway and alleviates disruption on blood-brain barrier following intracerebral haemorrhage in mice

Supplementary Material