Journal: Neoplasia (New York, N.Y.)

Article Title: Targeting PAR1 activation in JAK2V617F-driven philadelphia-negative myeloproliferative neoplasms: Unraveling its role in thrombosis and disease progression

doi: 10.1016/j.neo.2025.101153

Figure Lengend Snippet: Relative PAR1 gene expression analysis of (A) mononuclear cells ( p = 0.0005, Mann-Whitney U), (B) erythro‑myeloid restricted progenitors (EMPs, CD34+CD133-) ( p = 0.0008, Mann-Whitney U), (C) multipotent progenitor cells (MPPs, CD133+CD34+) ( p = 0.706, Mann-Whitney U), (D) hematopoietic and endothelial progenitor cells (HSC/ EPC, CD133-CD34-) ( p = 0.0002, Mann-Whitney U), (E) endothelial progenitor cells (EPCs, CD34-CD133+) ( p = 0.0064, Mann-Whitney U) in samples from 13 patients with myeloproliferative neoplasms and 5 control samples of cord blood. In each figure, the standard deviation of the mean (SD) is shown with a bar.

Article Snippet: The MNCs and/or CD45 - CD34 +/depleted cells of MPN patients or healthy volunteers were incubated with the combination of varying treatments including thrombin (Sigma Aldrich, St. Louis, Missouri, USA), selective PAR1 antagonist, Vorapaxar (SCH530348, MedChemExpress, Monmouth Junction, NJ, USA) and JAK2 inhibitor, Ruxolitinib (sc-364729, Santa Cruz Biotechnology, Dallas, Texas, USA) for the analysis.

Techniques: Gene Expression, MANN-WHITNEY, Control, Standard Deviation

Journal: Neoplasia (New York, N.Y.)

Article Title: Targeting PAR1 activation in JAK2V617F-driven philadelphia-negative myeloproliferative neoplasms: Unraveling its role in thrombosis and disease progression

doi: 10.1016/j.neo.2025.101153

Figure Lengend Snippet: JAK2V617F allele status of Mononuclear Cells and PAR1 sorted populations of Ph- MPN samples.

Article Snippet: The MNCs and/or CD45 - CD34 +/depleted cells of MPN patients or healthy volunteers were incubated with the combination of varying treatments including thrombin (Sigma Aldrich, St. Louis, Missouri, USA), selective PAR1 antagonist, Vorapaxar (SCH530348, MedChemExpress, Monmouth Junction, NJ, USA) and JAK2 inhibitor, Ruxolitinib (sc-364729, Santa Cruz Biotechnology, Dallas, Texas, USA) for the analysis.

Techniques:

Journal: Neoplasia (New York, N.Y.)

Article Title: Targeting PAR1 activation in JAK2V617F-driven philadelphia-negative myeloproliferative neoplasms: Unraveling its role in thrombosis and disease progression

doi: 10.1016/j.neo.2025.101153

Figure Lengend Snippet: PAR1 cell surface expression analysis of MPN cells (4 MPN patients with monoallelic JAK2V617F) (A) fluorescence-activated cell sorting plot with CD34 and PAR1 expression, (B and C) cell sorting according to CD34 and PAR1 expression that lack of CD45 expression. (D) EPCR cell surface expression analysis of MPN cells with CD34 expression.

Article Snippet: The MNCs and/or CD45 - CD34 +/depleted cells of MPN patients or healthy volunteers were incubated with the combination of varying treatments including thrombin (Sigma Aldrich, St. Louis, Missouri, USA), selective PAR1 antagonist, Vorapaxar (SCH530348, MedChemExpress, Monmouth Junction, NJ, USA) and JAK2 inhibitor, Ruxolitinib (sc-364729, Santa Cruz Biotechnology, Dallas, Texas, USA) for the analysis.

Techniques: Expressing, Fluorescence, FACS

Journal: Neoplasia (New York, N.Y.)

Article Title: Targeting PAR1 activation in JAK2V617F-driven philadelphia-negative myeloproliferative neoplasms: Unraveling its role in thrombosis and disease progression

doi: 10.1016/j.neo.2025.101153

Figure Lengend Snippet: The effect of thrombin on PAR1 expression was evaluated in (A) CD34 +/depleted cells who had lack of CD45 expression (B) the inhibitory effects of vorapaxar were tested in PAR1 cell surface expression (C) and on the phosphorylation of STAT-5B. GraphPad Prism 8.0 software was used for the statistical analysis. (Friedman Test; mean ± SEM, * P < 0.05, ** P < 0.01, ** P < 0.001).

Article Snippet: The MNCs and/or CD45 - CD34 +/depleted cells of MPN patients or healthy volunteers were incubated with the combination of varying treatments including thrombin (Sigma Aldrich, St. Louis, Missouri, USA), selective PAR1 antagonist, Vorapaxar (SCH530348, MedChemExpress, Monmouth Junction, NJ, USA) and JAK2 inhibitor, Ruxolitinib (sc-364729, Santa Cruz Biotechnology, Dallas, Texas, USA) for the analysis.

Techniques: Expressing, Software

Journal: Neoplasia (New York, N.Y.)

Article Title: Targeting PAR1 activation in JAK2V617F-driven philadelphia-negative myeloproliferative neoplasms: Unraveling its role in thrombosis and disease progression

doi: 10.1016/j.neo.2025.101153

Figure Lengend Snippet: The effect of PAR1 activation with thrombin in JAK2 pathway. Mononuclear cells obtained from MPN patients (n: 11) and healthy controls (n: 11) were cultured overnight in RPMI 1640 serum-free conditions and then treated with Ruxolitinib (300 nm, 3 h (monoallelic JAK2V617F) or 1.5 h (biallelic JAK2V617F and wild type), thrombin (1U, 1 h), vorapaxar (80uM, 1 h) to perform relative PAR1 gene expression analysis (A-I). In patients with monoallelic JAK2V617F (n: 4), biallelic JAK2V617F (n: 5) and wild type (n: 2), the effects of thrombin, vorapaxar and ruxolitinib administration on relative PAR1 gene expression were analyzed (J).

Article Snippet: The MNCs and/or CD45 - CD34 +/depleted cells of MPN patients or healthy volunteers were incubated with the combination of varying treatments including thrombin (Sigma Aldrich, St. Louis, Missouri, USA), selective PAR1 antagonist, Vorapaxar (SCH530348, MedChemExpress, Monmouth Junction, NJ, USA) and JAK2 inhibitor, Ruxolitinib (sc-364729, Santa Cruz Biotechnology, Dallas, Texas, USA) for the analysis.

Techniques: Activation Assay, Cell Culture, Gene Expression

Journal: Neoplasia (New York, N.Y.)

Article Title: Targeting PAR1 activation in JAK2V617F-driven philadelphia-negative myeloproliferative neoplasms: Unraveling its role in thrombosis and disease progression

doi: 10.1016/j.neo.2025.101153

Figure Lengend Snippet: The cell surface PAR1 expression pattern evaluated after treated MNC cells with thrombin (1U), vorapaxar (80uM), ruxolitinib (300 nm) healthy controls (n:11, p < 0.0001) (A), MPN patients (n:11, p < 0.0001) (B) and MPN patients have history of thrombosis (n:4, p:0.001) (C). Results are performed on two separate occasions. GraphPad Prism 8.0 software was used for the statistical analysis of cell surface protein expression data. (Friedmann Test).

Article Snippet: The MNCs and/or CD45 - CD34 +/depleted cells of MPN patients or healthy volunteers were incubated with the combination of varying treatments including thrombin (Sigma Aldrich, St. Louis, Missouri, USA), selective PAR1 antagonist, Vorapaxar (SCH530348, MedChemExpress, Monmouth Junction, NJ, USA) and JAK2 inhibitor, Ruxolitinib (sc-364729, Santa Cruz Biotechnology, Dallas, Texas, USA) for the analysis.

Techniques: Expressing, Software

Journal: Neoplasia (New York, N.Y.)

Article Title: Targeting PAR1 activation in JAK2V617F-driven philadelphia-negative myeloproliferative neoplasms: Unraveling its role in thrombosis and disease progression

doi: 10.1016/j.neo.2025.101153

Figure Lengend Snippet: The responses of MPN cells to PAR1 inhibition by detection of changes in PAR pathway. (A) Jak2V617F-induced PAR regulated genes and (C) trombin-PAR-coagulation suppressed genes affected >2-fold in the PAR pathway in mononuclear cells of MPN patients (2 patients with monoallelic JAK2V617F (p26 and p:29), 2 patients with biallelic JAK2V617F (p:64 and p:68) and no mutation carrying one patient (p: 35)) by PAR1 inhibition. (B) PAR pathway-related genes downregulated >2-fold in one MPN patient with history of thrombosis (p:26).

Article Snippet: The MNCs and/or CD45 - CD34 +/depleted cells of MPN patients or healthy volunteers were incubated with the combination of varying treatments including thrombin (Sigma Aldrich, St. Louis, Missouri, USA), selective PAR1 antagonist, Vorapaxar (SCH530348, MedChemExpress, Monmouth Junction, NJ, USA) and JAK2 inhibitor, Ruxolitinib (sc-364729, Santa Cruz Biotechnology, Dallas, Texas, USA) for the analysis.

Techniques: Inhibition, Coagulation, Mutagenesis

Journal: International journal of oncology

Article Title: Thrombin conducts epithelial‑mesenchymal transition via protease‑activated receptor‑1 in human gastric cancer.

doi: 10.3892/ijo.2014.2651

Figure Lengend Snippet: Figure 1. Protease‑activated receptor‑1 (PAR1) activation-dependent expression of epithelial‑mesenchymal transition (EMT) markers in MKN45/PAR1 and MKN74 cells. Whole‑cell and nuclear‑cell lysates of MKN45/mock, MKN45/PAR1 and MKN74 cells were probed for EMT‑marker expression by western blotting. (A) EMT‑marker expression remains the same in MKN45/mock cells treated with α‑thrombin or α‑thrombin plus SCH79797 for 24 h. (B) MKN45/PAR1 and MKN74 cells treated with α‑thrombin present decreased levels of E‑cadherin and β‑catenin and increased levels of fibronectin and vimentin in whole‑cell lysates over time. Nuclear lysates of these α‑thrombin‑treated cells presented an increase in β‑catenin over time suggesting movement of β‑catenin into the nucleus. (C) When treated with α‑thrombin and SCH79797, MKN45/PAR1 and MKN74 cells present results similar to MKN45/mock cells. Equal loading of protein was confirmed with anti‑GAPDH antibody.

Article Snippet: The selective PAR1 antagonist Sch79797 (catalog no. 1592) (ic50=70 nM) was purchased from tocris Bioscience (avonmouth, uK) (25).

Techniques: Activation Assay, Expressing, Western Blot

Journal: International journal of oncology

Article Title: Thrombin conducts epithelial‑mesenchymal transition via protease‑activated receptor‑1 in human gastric cancer.

doi: 10.3892/ijo.2014.2651

Figure Lengend Snippet: Figure 2. Fluorescence immunocytochemical staining of fibronectin and E‑cadherin in MKN45/mock, MKN45/PAR1 and MKN74 cells, when treated with α‑thrombin or α‑thrombin plus SCH79797. (A) MKN45/mock cells present no significant changes in fibronectin and E‑cadherin expression. (B) MKN45/APR1 and MKN74 cells treated with α‑thrombin presented a decreased level of E‑cadherin expression and an enhanced level of fibronectin expression. (C) MKN45/APR1 and MKN74 cells treated with α‑thrombin and SCH79797, presented fibronectin and E‑cadherin expression levels similar to that of untreated cultures of these cells.

Article Snippet: The selective PAR1 antagonist Sch79797 (catalog no. 1592) (ic50=70 nM) was purchased from tocris Bioscience (avonmouth, uK) (25).

Techniques: Fluorescence, Staining, Expressing

Journal: International journal of oncology

Article Title: Thrombin conducts epithelial‑mesenchymal transition via protease‑activated receptor‑1 in human gastric cancer.

doi: 10.3892/ijo.2014.2651

Figure Lengend Snippet: Figure 3. Electrophoretic mobility shift assays (EMSAs), demonstrate specific interaction with the E‑cadherin promoter. (A) EMSAs were performed with nuclear extracts from MKN45/mock and MKN74 cells and demonstrate an E‑cadherin E‑box 1‑3 nuclear protein complex. No levels of specific E‑box complexes are seen in MKN45/mock and MKN74 cells. These cells are the control. (B) These lanes show nuclear extracts from MKN45/PAR1 and MKN74 cells, treated with α‑thrombin for 12 h, and demonstrate an E‑cadherin E‑box1‑3 nuclear protein complex. Higher levels of specific E‑box complexes are seen in MKN45/PAR1 and MKN74 cells treated with α‑thrombin that overexpress relative to control cells. (C) Specific complexes were inhibited by protease‑activated receptor‑1 (PAR1) selective antagonist SCH79797.

Article Snippet: The selective PAR1 antagonist Sch79797 (catalog no. 1592) (ic50=70 nM) was purchased from tocris Bioscience (avonmouth, uK) (25).

Techniques: Electrophoretic Mobility Shift Assay, Control

Journal: International journal of oncology

Article Title: Thrombin conducts epithelial‑mesenchymal transition via protease‑activated receptor‑1 in human gastric cancer.

doi: 10.3892/ijo.2014.2651

Figure Lengend Snippet: Figure 4. Snail detected in nuclear lysate. The impact of α‑thrombin treatment of MKN45/PAR1 and MKN74 cells upon nuclear localization of transcription factors in these cells (Twist, Snail and E12/E47) was profiled by means of western blotting. Twist and E12/E47 were not able to migrate into the nucleus, when treated with α‑thrombin while Snail was able to do so, when these cells were treated with α‑thrombin for 12 h.

Article Snippet: The selective PAR1 antagonist Sch79797 (catalog no. 1592) (ic50=70 nM) was purchased from tocris Bioscience (avonmouth, uK) (25).

Techniques: Western Blot

Journal: Oncogene

Article Title: PAR1 inhibition suppresses the self-renewal and growth of A2B5-defined glioma progenitor cells and their derived gliomas in vivo

doi: 10.1038/onc.2015.452

Figure Lengend Snippet: PAR1 mRNA expression

Article Snippet: The selective PAR1 antagonists SCH 79797 and SCH 530348 were purchased, respectively from Tocris Bioscience (Ellisville, MO, USA) and Axon medchem (Axon 1755) and dissolved in DMSO as per the manufacturer’s instructions.

Techniques: Microarray

Journal: Oncogene

Article Title: PAR1 inhibition suppresses the self-renewal and growth of A2B5-defined glioma progenitor cells and their derived gliomas in vivo

doi: 10.1038/onc.2015.452

Figure Lengend Snippet: PAR1 is overexpressed in glioma tumor progenitor cells (TPCs) (a), Expression of PAR1 mRNA using real-time PCR, in freshly sorted glioma-derived A2B5+ TPCs (n = 12) relative to normal A2B5+ glial progenitor cells (GPCs) (n = 4) and unsorted cells (UNS) (n = 4), reveals that PAR1 mRNA was significantly upregulated at all stages of glioma development. (b–c) Relative quantification of PAR1 gene (b) and protein expression (c) using RT-PCR (b) and flow cytometry (c) detection in GBM-derived glioma-initiating cell lines (GICLs) established from unsorted or A2B5+ cells (*) maintained in serum-free media (SFM) supplemented with FGF, EGF (20 ng/ml) and PDGF (10 ng/ml) for less than 10 passages; and commercially available adherent GBM cells U87 and U251 (c) cultured in 10% serum culture conditions. Comparable quantities of cDNA were ensured by amplification of GAPDH (b). (d–f) Flow cytometry analysis of PAR1, A2B5 and CD133 expression in GBM-derived GICLs. Representative scatter plot of GICL8 stained with A2B5 (bottom right), PAR1 (upper left), both (upper right), or their corresponding isotype controls (bottom left) (D). Error bars indicate Means ± s.e.m.

Article Snippet: The selective PAR1 antagonists SCH 79797 and SCH 530348 were purchased, respectively from Tocris Bioscience (Ellisville, MO, USA) and Axon medchem (Axon 1755) and dissolved in DMSO as per the manufacturer’s instructions.

Techniques: Expressing, Real-time Polymerase Chain Reaction, Derivative Assay, Quantitative Proteomics, Reverse Transcription Polymerase Chain Reaction, Flow Cytometry, Cell Culture, Amplification, Staining

Journal: Oncogene

Article Title: PAR1 inhibition suppresses the self-renewal and growth of A2B5-defined glioma progenitor cells and their derived gliomas in vivo

doi: 10.1038/onc.2015.452

Figure Lengend Snippet: Analysis of PAR1 expression in relation with TCGA-defined glioblastoma subtypes and copy number variations (a–b), PAR1 gene expression was enriched in the CL subtype of GBM defined by the TCGA (n= 483) relative to normal brain tissue (n = 10) (a) but was not correlated with the glioma-Cpg Island Methylator Phenotype (G-CIMP) subtype. (b, c) Expression value of PAR1 gene expression in low-grade gliomas (n = 468) derived from the TCGA showing a significant enrichment of PAR1 in anaplastic AST, relative to grade II OLG and OA. Black lines in each group indicate mean ± s.e.m. 1 way ANOVA, P < 0.0001; *P < 0.05; **P < 0.01; ***P < 0.001 after Tukey’s multiple test comparison. (d) PAR1 expression was significantly correlated with EGFR, PTEN and CDKN2A copy number variations. AST, astrocytoma; CL, classical; OLG,: oligodendroglioma; OA, oligoastrocytoma; II and III: WHO grades II and III, respectively; MES, mesenchymal; NL, neural; PN: proneural.

Article Snippet: The selective PAR1 antagonists SCH 79797 and SCH 530348 were purchased, respectively from Tocris Bioscience (Ellisville, MO, USA) and Axon medchem (Axon 1755) and dissolved in DMSO as per the manufacturer’s instructions.

Techniques: Expressing, Gene Expression, Derivative Assay, Comparison

Journal: Oncogene

Article Title: PAR1 inhibition suppresses the self-renewal and growth of A2B5-defined glioma progenitor cells and their derived gliomas in vivo

doi: 10.1038/onc.2015.452

Figure Lengend Snippet: Lentiviral induced PAR1 knockdown (KD) validation. Validation of PAR1 gene (a, b, e) and protein (c–e) induced silencing using quantitative RT-PCR (a, b) and flow cytometry (c, d) A2B5+ derived glioma-initiating cell lines (GICLs), 6 days after transduction with two different PAR1 KD lentiviruses, compared with glioma cells transduced with a SCR. Gene expression levels normalized to GAPDH. One-way ANOVA with repeated measures; *P < 0.05; **P < 0.01; ***P < 0.001 after Tukey post-hoc comparisons. Means ± s.e.m.

Article Snippet: The selective PAR1 antagonists SCH 79797 and SCH 530348 were purchased, respectively from Tocris Bioscience (Ellisville, MO, USA) and Axon medchem (Axon 1755) and dissolved in DMSO as per the manufacturer’s instructions.

Techniques: Knockdown, Biomarker Discovery, Quantitative RT-PCR, Flow Cytometry, Derivative Assay, Transduction, Gene Expression

Journal: Oncogene

Article Title: PAR1 inhibition suppresses the self-renewal and growth of A2B5-defined glioma progenitor cells and their derived gliomas in vivo

doi: 10.1038/onc.2015.452

Figure Lengend Snippet: PAR1 silencing inhibits the growth and self-renewal of glioma TPCs. (a) Representative photomicrograph illustrating the number of A2B5+ TPCs derived from GICL-8 6 days after transduction with either PAR1-KD or control lentiviruses. Scale bar, 100 µm. (b–g) Effects of PAR1 silencing on the in vitro expansion (b, c), proliferation (d, e), survival (f, g) and clonal sphere formation (h, i) of A2B5+ TPCs derived from two glioma-initiating cell lines (GICL8 and GICL9), 6 days after transduction with different PAR1 knockdown (KD) lentiviruses, compared with scrambled lentivirus (SCR) and control (CT) untransduced cells. (b, c) Lentiviral KD of PAR1 significantly reduced the number of A2B5+ GICL relative to both SCR shRNAi-transduced and non-transduced CT cells. (d, e) EdU incorporation in association with propidium iodide (PI) staining revealed that GICLs subjected to PAR1 KD manifested fewer cells in S phase relative to SCR and CT cells. (f, g) PAR1 KD significantly increased the percentage of apoptotic cells as determined by flow cytometry analysis of Annexin V, relative to SCR and CT cells. KD, Knockdown. Means ± s.e.m. One-way ANOVA with repeated measures (P < 0.0001) with Tukey post-hoc comparisons. *P < 0.05; **P < 0.01; ***P < 0.001. Post-hoc comparisons between PAR1 KD cells and SCR and non-transduced control (CT) cells are illustrated by orange and black stars, respectively; three independent experiments for each cell line. (h, i) GICLs were plated into a 96-well plates for limiting dilution sphere formation assay, and counted 14 days later; wells were then scored for the presence or absence of sphere growth. The log fraction of the negative wells (non-responding) was plotted as a function of cell density per well.

Article Snippet: The selective PAR1 antagonists SCH 79797 and SCH 530348 were purchased, respectively from Tocris Bioscience (Ellisville, MO, USA) and Axon medchem (Axon 1755) and dissolved in DMSO as per the manufacturer’s instructions.

Techniques: Derivative Assay, Transduction, Control, In Vitro, Knockdown, Staining, Flow Cytometry, Tube Formation Assay

Journal: Oncogene

Article Title: PAR1 inhibition suppresses the self-renewal and growth of A2B5-defined glioma progenitor cells and their derived gliomas in vivo

doi: 10.1038/onc.2015.452

Figure Lengend Snippet: PAR1 silencing suppresses the in vivo growth of TPC-derived tumors and prolongs survival Effects of PAR1 silencing on the in vivo expansion of A2B5+ GICLs derived from two different GBM (28 000 cells per animal, n = 5–6 mice per group), 4 weeks after transduction with PAR1 knockdown (KD) lentiviruses, compared with scrambled lentivirus (SCR) and control (CT) untransduced cells. (a) Hematoxylin-eosin stained sections of xenografts following intracranial implantation of A2B5+ TPCs. (b–g) Graphs representing the stereological analysis of the tumor extension, measured along the antero-posterior axis of xenograft mice brain (b, c); tumor volume (d, e); and proliferation of glioma TPCs as shown by the number of xenografted cells stained with the anti-human nuclei antigen (HNA) co-expressing the mitotic marker Ki67 (f, g), demonstrating a prominent inhibitory effect of PAR1 silencing on the tumorigenicity and mitotic activity of glioma A2B5+ TPCs relative to SCR and CT cells. Means ± s.e.m. P-values calculated using one-way ANOVA (P < 0.0001) followed by Tukey post-hoc comparisons with *P < 0.05; **P < 0.01; ***P < 0.001. Post-hoc comparisons between cells transduced with PAR1 KD shRNAi, compared with those transduced with SCR shRNAi untransduced CT cells are illustrated by orange and black stars, respectively. (h–i) Kaplan–Meier curves show an increase in median survival of mice bearing intracranial glioma TPCs transduced with PAR1 shRNA relative to SCR and CT mice. Log-rank analysis, (P < 0.0001) followed by pairwise comparison between all groups with **P < 0.01 and ***P < 0.001.

Article Snippet: The selective PAR1 antagonists SCH 79797 and SCH 530348 were purchased, respectively from Tocris Bioscience (Ellisville, MO, USA) and Axon medchem (Axon 1755) and dissolved in DMSO as per the manufacturer’s instructions.

Techniques: In Vivo, Derivative Assay, Transduction, Knockdown, Control, Staining, Expressing, Marker, Activity Assay, shRNA, Comparison

Journal: Oncogene

Article Title: PAR1 inhibition suppresses the self-renewal and growth of A2B5-defined glioma progenitor cells and their derived gliomas in vivo

doi: 10.1038/onc.2015.452

Figure Lengend Snippet: Pharmacological inhibition of PAR1 impedes glioma TPC expansion and migration in vitro. Effects of the specific PAR1 inhibitors SCH79797 and SCH530348 on the in vitro expansion (a–d) and migration (e–h) of A2B5+ GICL derived from GBMs. Dose-dependent growth of GBM-derived TPCs was measured by counting the number of cells 4 days after administration of SCH79797 (a, b) and SCH530348 (c, d) relative to highest concentration of vehicle control (DMSO). P-values were calculated using one-way ANOVA with repeated measures followed by Tukey post-hoc comparisons with *P < 0.05; **P < 0.01; ***P < 0.001. Results were obtained from three independent experiments for each cell line. Migration was measured by assessing the average cell speed of A2B5+ GICLs in a dose-dependent manner, 24 h after administration of SCH79797 (e, f) and SCH530348 (g, h), relative to 1% DMSO vehicle control solution. P-values were calculated using Kruskal–Wallis test followed by Dunn’s multiple comparison test post-hoc comparisons with **P < 0.01; ***P < 0.001. Means ± s.e.m.

Article Snippet: The selective PAR1 antagonists SCH 79797 and SCH 530348 were purchased, respectively from Tocris Bioscience (Ellisville, MO, USA) and Axon medchem (Axon 1755) and dissolved in DMSO as per the manufacturer’s instructions.

Techniques: Inhibition, Migration, In Vitro, Derivative Assay, Concentration Assay, Control, Comparison