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Additional Supporting Information can be found in the online version of this article.

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ANA_22549_sm_SuppFig1AB.tif1473KSupplemental Figure 1: Immunofluorescence for the expression of MMP-9, MMP-10, MMP-13 and phospho-p38 MAPK in the astrocytes and endothelial cells in the perihematomal area 6 hours following bICH. Representative photographs of immunofluorescence staining revealed that MMP-9 (A), MMP-13 (C) and phosphor-p38 (D) (red) expressed in astrocytes (GFAP, green) and endothelial cells (vWf, green), and MMP-10 (B) expressed in endothelial cells (vWf, green). Scale bar: 50 μm.
ANA_22549_sm_SuppFig1CD.tif1473KSupplemental Figure 1: Immunofluorescence for the expression of MMP-9, MMP-10, MMP-13 and phospho-p38 MAPK in the astrocytes and endothelial cells in the perihematomal area 6 hours following bICH. Representative photographs of immunofluorescence staining revealed that MMP-9 (A), MMP-13 (C) and phosphor-p38 (D) (red) expressed in astrocytes (GFAP, green) and endothelial cells (vWf, green), and MMP-10 (B) expressed in endothelial cells (vWf, green). Scale bar: 50 μm.
ANA_22549_sm_SuppFig2.tif994KSupplemental Figure 2: PDGFR-α activation failed to exacerbate neurobehavioral functions (A, B), but increased brain edema in bICH mice (C). Modified Garcia test (A) and corner turn (B) at 24 hours following operation in sham, vehicle and PDGF-AA treatment (200 ng) mice; (C) Brain edema 24 hours following operation in sham, vehicle and PDGF-AA treatment (200 ng) mice; # p < 0.05 vs Sham; * p < 0.05 vs Vehicle. n = 7-12 mice per group. Error bars represent median ± 25th-75th percentiles (A) or mean ± standard error of the mean (B and C). # p < 0.05 vs Sham; * p < 0.05 vs Vehicle.
ANA_22549_sm_SuppFig3.tif468KSupplemental Figure 3: Thrombin inhibition improved neurobehavioral functions following bICH injury. Modified Garcia test (A) and corner turn (B) 24 hours following operation in sham, vehicle and hirudin treatment (5 U) mice. n = 7 mice per group. Error bars represent median ± 25th-75th percentiles (A) or mean ± standard error of the mean (B). # p < 0.05 vs Sham; * p < 0.05 vs Vehicle.
ANA_22549_sm_SuppFig4.tif457KSupplemental Figure 4: Activation of PDGFR-α by PDGF-AA reversed thrombin inhibition by hirudin following Bich. Modified Garcia test (A) and corner turn (B) 24 hours after bICH in hirudin (5 U) and hirudin (5 U)+PDGF-AA (200 ng) mice. n = 7 mice per group. Error bars represent median ± 25th-75th percentiles (A) or mean ± standard error of the mean (B). & p < 0.05 vs Hirudin.
ANA_22549_sm_SuppFig5.tif1256KSupplemental Figure 5: Characterization of the PDGFR-α downstream pathway at 6 hours following thrombin injection in mice. (A) Zymography assay for MMP-9 and MMP-2 activity in the ipsilateral hemisphere in sham, thrombin and Gl treatment (60 mg/kg) mice; Western blot assay for MMP-10 (D), MMP-13 (F), and p38/p-p38 (H), p-ATF-2 (J) in the ipsilateral hemisphere in sham, thrombin and Gl treatment (60 mg/kg) mice. Quantification of A, D, F, H and J is shown in B, C, E, G, I and K, respectively, n = 5-8 mice per group. Error bars represent mean ± standard error of the mean. # p < 0.05 vs Sham; * p < 0.05 vs Thrombin.
ANA_22549_sm_SuppFig6.tif2542KSupplemental Figure 6: Schematic of PDGFR-α signaling pathway triggered by thrombin post-ICH. Thrombin promotes PDGFR-α activation via upregulation of PDGF-AA, leading to p38 MAPK signaling but not ERK or JNK MAPKs signaling, and subsequent activation of downstream transcription factor, ATF-2. Activation of ATF-2 results in expression of MMPs which degrade extracellular matrix and finally lead to BBB disruption.
ANA_22549_sm_SuppInfo.doc50KSupporting Information

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