Review

mouse anti human par2 antibody (Santa Cruz Biotechnology)

Santa Cruz Biotechnology is a verified supplier

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Santa Cruz Biotechnology mouse anti human par2 antibody

Examination of the mechanism of influence of TF on Tau protein expression and phosphorylation in differentiated SH-SY5Y cells. SH-SY5Y (2 × 10 5 ) were treated with recombinant relipidated Innovin TF (0.65 ng/ml) together with or without human fVIIa (5 nM) or fVIIa alone. In some experiments, the TF aliquots were pre-incubated for 1 h, with 10H10 antibody (20 µg/ml) capable of blocking TF signalling, HTF-1 antibody (20 µg/ml) to block TF-fVIIa protease/procoagulant activity, or a mouse control isotype IgG antibody (20 µg/ml; not shown). In other experiments, fVIIa was pre-incubated for 1 h with the chemical inhibitor PCI27483 (10 µg/ml). Alternatively, the neuronal cells were treated with AIIB2 antibody (20 µg/ml) to block β1-integrin signalling, SAM11 antibody (20 µg/ml) capable of blocking <t>PAR2</t> signalling, or PAR2-activating peptide (PAR2-AP; 20 µM) to induce PAR2 signalling. Cells were harvested at 24 h, and cellular lysates (10 µg protein) were examined for Tau and phospho-Thr181 Tau by western blot analysis. All values were normalised against the respective GAPDH and for comparison, all ratios were calculated against the average from the non-treated cells ± the calculated standard deviation. The number of experiments is shown in each column, and all data groups were determined to have normal distributions and are shown in each column. A SH-SY5Y protein electrophoresis, B SH-SY5Y phospho-Thr181 Tau electrophoresis, C SH-SY5Y Tau protein ratio, and D SH-SY5Y phospho-Thr181 Tau ratio

Mouse Anti Human Par2 Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 491 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mouse anti human par2 antibody/product/Santa Cruz Biotechnology
Average 94 stars, based on 491 article reviews

mouse anti human par2 antibody - by Bioz Stars, 2026-05

94/100 stars

Images

1) Product Images from "Procoagulant Extracellular Vesicles Increase Neuronal Tau expression, Metabolism and Processing Through Tissue Factor and Protease Activated Receptor 2"

Article Title: Procoagulant Extracellular Vesicles Increase Neuronal Tau expression, Metabolism and Processing Through Tissue Factor and Protease Activated Receptor 2

Journal: Cellular and Molecular Neurobiology

doi: 10.1007/s10571-025-01658-7

Figure Legend Snippet: Examination of the mechanism of influence of TF on Tau protein expression and phosphorylation in differentiated SH-SY5Y cells. SH-SY5Y (2 × 10 5 ) were treated with recombinant relipidated Innovin TF (0.65 ng/ml) together with or without human fVIIa (5 nM) or fVIIa alone. In some experiments, the TF aliquots were pre-incubated for 1 h, with 10H10 antibody (20 µg/ml) capable of blocking TF signalling, HTF-1 antibody (20 µg/ml) to block TF-fVIIa protease/procoagulant activity, or a mouse control isotype IgG antibody (20 µg/ml; not shown). In other experiments, fVIIa was pre-incubated for 1 h with the chemical inhibitor PCI27483 (10 µg/ml). Alternatively, the neuronal cells were treated with AIIB2 antibody (20 µg/ml) to block β1-integrin signalling, SAM11 antibody (20 µg/ml) capable of blocking PAR2 signalling, or PAR2-activating peptide (PAR2-AP; 20 µM) to induce PAR2 signalling. Cells were harvested at 24 h, and cellular lysates (10 µg protein) were examined for Tau and phospho-Thr181 Tau by western blot analysis. All values were normalised against the respective GAPDH and for comparison, all ratios were calculated against the average from the non-treated cells ± the calculated standard deviation. The number of experiments is shown in each column, and all data groups were determined to have normal distributions and are shown in each column. A SH-SY5Y protein electrophoresis, B SH-SY5Y phospho-Thr181 Tau electrophoresis, C SH-SY5Y Tau protein ratio, and D SH-SY5Y phospho-Thr181 Tau ratio

Techniques Used: Expressing, Phospho-proteomics, Recombinant, Incubation, Blocking Assay, Activity Assay, Control, Western Blot, Comparison, Standard Deviation, Protein Electrophoresis, Electrophoresis

Time-course analysis of the Tau protein fragments in differentiated SH-SY5Y cells, following treatment with TF . SH-SY5Y (2 × 10 5 ) were treated with as single dose of recombinant relipidated Innovin TF (0.65 ng/ml) together with human fVIIa (5 nM). In some experiments, the TF aliquots were pre-incubated for 1 h, with 10H10 antibody (20 µg/ml) capable of blocking TF signalling, HTF-1 antibody (20 µg/ml) to block TF-fVIIa protease/procoagulant activity, or a mouse control isotype IgG antibody (20 µg/ml; not shown). Alternatively, the neuronal cells were treated with AIIB2 antibody (20 µg/ml) to block β1-integrin signalling, or SAM11 antibody (20 µg/ml) capable of blocking PAR2 signalling. Sets of cells were harvested at A 48 h and D at 72 h and cellular lysates (10 µg protein) were examined for Tau by western blot analysis. All values were normalised against the respective GAPDH (see Supplementary Fig. 6 A and B) and for comparison, all ratios were calculated against the average from the non-treated cells ± the calculated standard deviation. The data were obtained from 6 biological experiments, and all data groups were determined to have normal distributions. A Electrophoresis at 48 h, B calculated ratios of 50 kDa bands at 48 h, C calculated ratios of 30–35 kDa bands at 48 h, D electrophoresis at 72 h, E calculated ratios of 50 kDa bands at 72 h, F calculated ratios of 40 kDa bands at 72 h, G calculated ratios of 30–35 kDa bands at 72 h

Figure Legend Snippet: Time-course analysis of the Tau protein fragments in differentiated SH-SY5Y cells, following treatment with TF . SH-SY5Y (2 × 10 5 ) were treated with as single dose of recombinant relipidated Innovin TF (0.65 ng/ml) together with human fVIIa (5 nM). In some experiments, the TF aliquots were pre-incubated for 1 h, with 10H10 antibody (20 µg/ml) capable of blocking TF signalling, HTF-1 antibody (20 µg/ml) to block TF-fVIIa protease/procoagulant activity, or a mouse control isotype IgG antibody (20 µg/ml; not shown). Alternatively, the neuronal cells were treated with AIIB2 antibody (20 µg/ml) to block β1-integrin signalling, or SAM11 antibody (20 µg/ml) capable of blocking PAR2 signalling. Sets of cells were harvested at A 48 h and D at 72 h and cellular lysates (10 µg protein) were examined for Tau by western blot analysis. All values were normalised against the respective GAPDH (see Supplementary Fig. 6 A and B) and for comparison, all ratios were calculated against the average from the non-treated cells ± the calculated standard deviation. The data were obtained from 6 biological experiments, and all data groups were determined to have normal distributions. A Electrophoresis at 48 h, B calculated ratios of 50 kDa bands at 48 h, C calculated ratios of 30–35 kDa bands at 48 h, D electrophoresis at 72 h, E calculated ratios of 50 kDa bands at 72 h, F calculated ratios of 40 kDa bands at 72 h, G calculated ratios of 30–35 kDa bands at 72 h

Techniques Used: Recombinant, Incubation, Blocking Assay, Activity Assay, Control, Western Blot, Comparison, Standard Deviation, Electrophoresis

Image Search Results

Journal: Cellular and Molecular Neurobiology

Article Title: Procoagulant Extracellular Vesicles Increase Neuronal Tau expression, Metabolism and Processing Through Tissue Factor and Protease Activated Receptor 2

doi: 10.1007/s10571-025-01658-7

Figure Lengend Snippet: Examination of the mechanism of influence of TF on Tau protein expression and phosphorylation in differentiated SH-SY5Y cells. SH-SY5Y (2 × 10 5 ) were treated with recombinant relipidated Innovin TF (0.65 ng/ml) together with or without human fVIIa (5 nM) or fVIIa alone. In some experiments, the TF aliquots were pre-incubated for 1 h, with 10H10 antibody (20 µg/ml) capable of blocking TF signalling, HTF-1 antibody (20 µg/ml) to block TF-fVIIa protease/procoagulant activity, or a mouse control isotype IgG antibody (20 µg/ml; not shown). In other experiments, fVIIa was pre-incubated for 1 h with the chemical inhibitor PCI27483 (10 µg/ml). Alternatively, the neuronal cells were treated with AIIB2 antibody (20 µg/ml) to block β1-integrin signalling, SAM11 antibody (20 µg/ml) capable of blocking PAR2 signalling, or PAR2-activating peptide (PAR2-AP; 20 µM) to induce PAR2 signalling. Cells were harvested at 24 h, and cellular lysates (10 µg protein) were examined for Tau and phospho-Thr181 Tau by western blot analysis. All values were normalised against the respective GAPDH and for comparison, all ratios were calculated against the average from the non-treated cells ± the calculated standard deviation. The number of experiments is shown in each column, and all data groups were determined to have normal distributions and are shown in each column. A SH-SY5Y protein electrophoresis, B SH-SY5Y phospho-Thr181 Tau electrophoresis, C SH-SY5Y Tau protein ratio, and D SH-SY5Y phospho-Thr181 Tau ratio

Article Snippet: Alternatively, the neuronal cells were treated with a rat anti-human antibody (20 μg/ml; AIIB2; Merck KGaA) to block β1-integrin signalling, a mouse anti-human PAR2 antibody, SAM11 (20 μg/ml; Santa Cruz Biotechnology, Heidelberg, Germany), capable of blocking PAR2 signalling, or PAR2-activating peptide (PAR2-AP; 20 μM) to induce PAR2 signalling.

Techniques: Expressing, Phospho-proteomics, Recombinant, Incubation, Blocking Assay, Activity Assay, Control, Western Blot, Comparison, Standard Deviation, Protein Electrophoresis, Electrophoresis

Journal: Cellular and Molecular Neurobiology

Article Title: Procoagulant Extracellular Vesicles Increase Neuronal Tau expression, Metabolism and Processing Through Tissue Factor and Protease Activated Receptor 2

doi: 10.1007/s10571-025-01658-7

Figure Lengend Snippet: Time-course analysis of the Tau protein fragments in differentiated SH-SY5Y cells, following treatment with TF . SH-SY5Y (2 × 10 5 ) were treated with as single dose of recombinant relipidated Innovin TF (0.65 ng/ml) together with human fVIIa (5 nM). In some experiments, the TF aliquots were pre-incubated for 1 h, with 10H10 antibody (20 µg/ml) capable of blocking TF signalling, HTF-1 antibody (20 µg/ml) to block TF-fVIIa protease/procoagulant activity, or a mouse control isotype IgG antibody (20 µg/ml; not shown). Alternatively, the neuronal cells were treated with AIIB2 antibody (20 µg/ml) to block β1-integrin signalling, or SAM11 antibody (20 µg/ml) capable of blocking PAR2 signalling. Sets of cells were harvested at A 48 h and D at 72 h and cellular lysates (10 µg protein) were examined for Tau by western blot analysis. All values were normalised against the respective GAPDH (see Supplementary Fig. 6 A and B) and for comparison, all ratios were calculated against the average from the non-treated cells ± the calculated standard deviation. The data were obtained from 6 biological experiments, and all data groups were determined to have normal distributions. A Electrophoresis at 48 h, B calculated ratios of 50 kDa bands at 48 h, C calculated ratios of 30–35 kDa bands at 48 h, D electrophoresis at 72 h, E calculated ratios of 50 kDa bands at 72 h, F calculated ratios of 40 kDa bands at 72 h, G calculated ratios of 30–35 kDa bands at 72 h

Techniques: Recombinant, Incubation, Blocking Assay, Activity Assay, Control, Western Blot, Comparison, Standard Deviation, Electrophoresis

APC inhibits DNFB-induced ear thickness in WT and PAR1KO, but not in PAR2KO mice. CHS was induced via DNFB challenge on the flank skin on day zero and day one, then on the dorsum of both ears on day five to day 13 in mice. The ear thickness was measured from day zero to day 14. ( A ) The ear thickness of WT, PAR1KO and PAR2KO mice challenged with DNFB or solvent (NEGATIVE). ( B – E ) The ear thickness of mice challenged with DNFB and therapeutically treated with PAR1 activated peptide (WT + PAR1AP) or scramble control peptide (WT + SC) (10 mg/kg) in WT mice, APC (2 mg/kg) or PBS in WT (WT APC, WT PBS), PAR1KO (PAR1KO APC, PAR1KO PBS) or PAR2KO (PAR2KO APC, PAR2KO PBS) mice. ( F – H ) The ear thickness of WT, PAR1KO and PAR2KO mice challenged with DNFB and preventatively treated with APC (2 mg/kg) or PBS. Data shown on graph are means ± SD ( n = 8 for all groups).

Journal: International Journal of Molecular Sciences

Article Title: Activated Protein C Protects against Murine Contact Dermatitis by Suppressing Protease-Activated Receptor 2

doi: 10.3390/ijms23010516

Figure Lengend Snippet: APC inhibits DNFB-induced ear thickness in WT and PAR1KO, but not in PAR2KO mice. CHS was induced via DNFB challenge on the flank skin on day zero and day one, then on the dorsum of both ears on day five to day 13 in mice. The ear thickness was measured from day zero to day 14. ( A ) The ear thickness of WT, PAR1KO and PAR2KO mice challenged with DNFB or solvent (NEGATIVE). ( B – E ) The ear thickness of mice challenged with DNFB and therapeutically treated with PAR1 activated peptide (WT + PAR1AP) or scramble control peptide (WT + SC) (10 mg/kg) in WT mice, APC (2 mg/kg) or PBS in WT (WT APC, WT PBS), PAR1KO (PAR1KO APC, PAR1KO PBS) or PAR2KO (PAR2KO APC, PAR2KO PBS) mice. ( F – H ) The ear thickness of WT, PAR1KO and PAR2KO mice challenged with DNFB and preventatively treated with APC (2 mg/kg) or PBS. Data shown on graph are means ± SD ( n = 8 for all groups).

Article Snippet: Human foreskins and mouse skin tissue sections were de-paraffinized and subjected to immunostaining using rabbit anti-human or mouse PAR1 antibody, goat anti-human or mouse PAR2 antibody (Santa Cruz Biotech, Dallas, TX, USA), or anti-rabbit or anti-goat IgG (negative controls), followed by in the appropriate ready-to-use secondary antibody, and then the Liquid DAB+ Substrate Chromogen System (Agilent DAKO, Santa Clara, CA, USA).

Techniques: Solvent, Control

PAR1 and PAR2 expression in skin epidermis. PAR1 and PAR2 in the skin tissues were detected by immunostaining. ( A ) Representative images of PAR1 and PAR2 in skin tissues from newborn or adult WT, PAR1KO or PAR2KO mice. Scale bar: 100 µm. ( B , C ) Representative images of PAR1 and PAR2 in human neonatal foreskin ( B ), or in the ear skin from normal WT mice or WT mice with CHS treated with APC (2 mg/mL, APC + CHS) or PBS (PBS + CHS). Scale bar: 50 µm. CA: cartilage; EP: epidermis; DM: dermis; HF: hair follicle. Arrows indicate positive staining.

Journal: International Journal of Molecular Sciences

Article Title: Activated Protein C Protects against Murine Contact Dermatitis by Suppressing Protease-Activated Receptor 2

doi: 10.3390/ijms23010516

Figure Lengend Snippet: PAR1 and PAR2 expression in skin epidermis. PAR1 and PAR2 in the skin tissues were detected by immunostaining. ( A ) Representative images of PAR1 and PAR2 in skin tissues from newborn or adult WT, PAR1KO or PAR2KO mice. Scale bar: 100 µm. ( B , C ) Representative images of PAR1 and PAR2 in human neonatal foreskin ( B ), or in the ear skin from normal WT mice or WT mice with CHS treated with APC (2 mg/mL, APC + CHS) or PBS (PBS + CHS). Scale bar: 50 µm. CA: cartilage; EP: epidermis; DM: dermis; HF: hair follicle. Arrows indicate positive staining.

Techniques: Expressing, Immunostaining, Staining

Normal mouse aortic arch (Ldlr−/− mice fed a chow ® diet for 24 weeks) or atherosclerosis-containing aortic arches (Ldlr−/− mice fed a ‘Western’ diet for 24 weeks) were examined for (A) mRNA extrapolated to normal and (B) protein expression (n = 5 individual samples/group). Normal or diseased human carotid arteries were isolated and examined for (C) mRNA extrapolated to normal and (D) protein expression (n = 5 individual samples/group). Immunologic detection of PAR2 expression was also performed on mouse atherosclerotic aortic sinus (E – F) and human carotid atherosclerotic lesions (H – I; n = 4 – 5 individual samples/species; 4 x mag E & H; 10 x mag F & I). (G & J) Quantification of PAR2 staining in the lesion or media of atherosclerotic lesions. Solid white box is zoomed in area. Dashed white line is the area of the lesion. Histobars represent mean ± SEM. * Denotes P < 0.05 for comparisons to normal aorta/artery or lesion versus tunica media (Two-tailed Student’s t-test).

Journal: Arteriosclerosis, thrombosis, and vascular biology

Article Title: Protease-activated Receptor 2 Deficiency Attenuates Atherosclerosis in Mice

doi: 10.1161/ATVBAHA.117.310082

Figure Lengend Snippet: Normal mouse aortic arch (Ldlr−/− mice fed a chow ® diet for 24 weeks) or atherosclerosis-containing aortic arches (Ldlr−/− mice fed a ‘Western’ diet for 24 weeks) were examined for (A) mRNA extrapolated to normal and (B) protein expression (n = 5 individual samples/group). Normal or diseased human carotid arteries were isolated and examined for (C) mRNA extrapolated to normal and (D) protein expression (n = 5 individual samples/group). Immunologic detection of PAR2 expression was also performed on mouse atherosclerotic aortic sinus (E – F) and human carotid atherosclerotic lesions (H – I; n = 4 – 5 individual samples/species; 4 x mag E & H; 10 x mag F & I). (G & J) Quantification of PAR2 staining in the lesion or media of atherosclerotic lesions. Solid white box is zoomed in area. Dashed white line is the area of the lesion. Histobars represent mean ± SEM. * Denotes P < 0.05 for comparisons to normal aorta/artery or lesion versus tunica media (Two-tailed Student’s t-test).

Article Snippet: HRP-conjugated monoclonal mouse anti-human PAR2 (SAM-11, Santa Cruz, catalog #sc-13504 HRP) was added to each well (1:1000 dilution in 1x PBS/0.2% BSA/0.1% Triton X-100, 50 μl/well) and incubated for 1 hour at 37oC.

Techniques: Western Blot, Expressing, Isolation, Staining, Two Tailed Test

Male and female Ldlr−/− mice that were Par2+/+ and −/− (n = 16 – 30) were fed a high fat/cholesterol diet for 12 weeks. (A) Percent lesion area of the aortic sinus and (B) en face area of the aortic arch where circles represent individual measurements, diamonds are means ± SEM. * Denotes P = 0.001 for comparisons of −/− to +/+ (Two-way ANOVA with Holm-sidak post hoc). (C,D) Representative images of Oil-red O stained aortic sinus and (E,F) unstained en face images of the aortic arch. Representative images and quantification of (G) CD68, (H) SMC α-actin, and (I) picrosirius red stained aortic sinus lesions (Ldlr−/−/Par2+/+ - top; Ldlr−/−/Par2−/− - bottom). Histobars represent means ± SEM. ** Denotes P < 0.005 for comparison of −/− to +/+ (two-tailed Student’s t-test). ╪ Denotes P < 0.001 for comparison of −/− to +/+ and † denotes P < 0.05 for comparison of +/+ to −/− (One way ANOVA on Ranks with Dunn’s post hoc).

Journal: Arteriosclerosis, thrombosis, and vascular biology

Article Title: Protease-activated Receptor 2 Deficiency Attenuates Atherosclerosis in Mice

doi: 10.1161/ATVBAHA.117.310082

Figure Lengend Snippet: Male and female Ldlr−/− mice that were Par2+/+ and −/− (n = 16 – 30) were fed a high fat/cholesterol diet for 12 weeks. (A) Percent lesion area of the aortic sinus and (B) en face area of the aortic arch where circles represent individual measurements, diamonds are means ± SEM. * Denotes P = 0.001 for comparisons of −/− to +/+ (Two-way ANOVA with Holm-sidak post hoc). (C,D) Representative images of Oil-red O stained aortic sinus and (E,F) unstained en face images of the aortic arch. Representative images and quantification of (G) CD68, (H) SMC α-actin, and (I) picrosirius red stained aortic sinus lesions (Ldlr−/−/Par2+/+ - top; Ldlr−/−/Par2−/− - bottom). Histobars represent means ± SEM. ** Denotes P < 0.005 for comparison of −/− to +/+ (two-tailed Student’s t-test). ╪ Denotes P < 0.001 for comparison of −/− to +/+ and † denotes P < 0.05 for comparison of +/+ to −/− (One way ANOVA on Ranks with Dunn’s post hoc).

Techniques: Staining, Comparison, Two Tailed Test

Metabolic and lipid parameters from study mice

Journal: Arteriosclerosis, thrombosis, and vascular biology

Article Title: Protease-activated Receptor 2 Deficiency Attenuates Atherosclerosis in Mice

doi: 10.1161/ATVBAHA.117.310082

Figure Lengend Snippet: Metabolic and lipid parameters from study mice

Techniques:

Male Ldlr−/−/Par2+/+ and Ldlr−/−/Par2−/− mice (8–10 weeks old, n = 10 – 12 each group) were irradiated (1300 rads split into two equal doses four hours apart) and repopulated with Par2+/+ or −/− bone marrow. Mice were allowed to recover for 5 weeks, and then fed a Western diet for 12 weeks. (A) Percent lesion area of the aortic sinus and (B) en face area of the aortic arch where circles represent individual measurements, diamonds are means ± SEM. (C) Representative images of unstained en face images of the aortic arch. Representative images and quantification of (D) CD68, (E) SMC α-actin, and (F) picrosirius red stained aortic sinus lesions. Histobars represent means ± SEM. * Denotes P = 0.001, ** denotes P < 0.05 for comparisons of −/− to +/+; † denotes P < 0.05 for comparison of +/+ to −/− (A, B, D: Two-way ANOVA with Holm-sidak post hoc; C, E: Two-way ANOVA on Ranks Dunn’s post hoc).

Journal: Arteriosclerosis, thrombosis, and vascular biology

Article Title: Protease-activated Receptor 2 Deficiency Attenuates Atherosclerosis in Mice

doi: 10.1161/ATVBAHA.117.310082

Figure Lengend Snippet: Male Ldlr−/−/Par2+/+ and Ldlr−/−/Par2−/− mice (8–10 weeks old, n = 10 – 12 each group) were irradiated (1300 rads split into two equal doses four hours apart) and repopulated with Par2+/+ or −/− bone marrow. Mice were allowed to recover for 5 weeks, and then fed a Western diet for 12 weeks. (A) Percent lesion area of the aortic sinus and (B) en face area of the aortic arch where circles represent individual measurements, diamonds are means ± SEM. (C) Representative images of unstained en face images of the aortic arch. Representative images and quantification of (D) CD68, (E) SMC α-actin, and (F) picrosirius red stained aortic sinus lesions. Histobars represent means ± SEM. * Denotes P = 0.001, ** denotes P < 0.05 for comparisons of −/− to +/+; † denotes P < 0.05 for comparison of +/+ to −/− (A, B, D: Two-way ANOVA with Holm-sidak post hoc; C, E: Two-way ANOVA on Ranks Dunn’s post hoc).

Techniques: Irradiation, Western Blot, Staining, Comparison

Male Ldlr−/− mice (8–12 weeks) that were Par2+/+ and −/− (n = 12) were fed a high fat/cholesterol diet for 24 weeks. (A) Percent lesion area of the aortic sinus and (B) en face area of the aortic arch where circles represent individual measurements, diamonds are means ± SEM. (C–D and F–G) Sirius red stain for collagen at 40x magnification (C,D) and 200x magnification (D,G). Yellow * and # represent secondary atherosclerotic lesions and necrotic core, respectively. (E,H) SMC α-actin immunofluorescence where yellow arrows highlight the SMC cap in the −/− mice. Quantification of (I) aortic sinus lesion collagen, SMC, necrotic core, and CD68; (J) fibrous cap thickness; and (K) fibrous cap composition of collagen and SMC α-actin). Histobars represent means ± SEM. * Denotes P = 0.001 (Mann-Whitney Rank Sum), ╪ denotes P < 0.05 (Mann Whitney U test), ** P < 0.05 (ANOVA on ranks Dunn’s post hoc) for comparisons of −/− to +/+.

Journal: Arteriosclerosis, thrombosis, and vascular biology

Article Title: Protease-activated Receptor 2 Deficiency Attenuates Atherosclerosis in Mice

doi: 10.1161/ATVBAHA.117.310082

Figure Lengend Snippet: Male Ldlr−/− mice (8–12 weeks) that were Par2+/+ and −/− (n = 12) were fed a high fat/cholesterol diet for 24 weeks. (A) Percent lesion area of the aortic sinus and (B) en face area of the aortic arch where circles represent individual measurements, diamonds are means ± SEM. (C–D and F–G) Sirius red stain for collagen at 40x magnification (C,D) and 200x magnification (D,G). Yellow * and # represent secondary atherosclerotic lesions and necrotic core, respectively. (E,H) SMC α-actin immunofluorescence where yellow arrows highlight the SMC cap in the −/− mice. Quantification of (I) aortic sinus lesion collagen, SMC, necrotic core, and CD68; (J) fibrous cap thickness; and (K) fibrous cap composition of collagen and SMC α-actin). Histobars represent means ± SEM. * Denotes P = 0.001 (Mann-Whitney Rank Sum), ╪ denotes P < 0.05 (Mann Whitney U test), ** P < 0.05 (ANOVA on ranks Dunn’s post hoc) for comparisons of −/− to +/+.

Techniques: Staining, Immunofluorescence, MANN-WHITNEY

Plasma cytokines were analyzed from aforementioned (A) 12 and 24 week ‘Western’ diet fed Ldlr−/−/Par2+/+ and Ldlr−/−/Par2−/− mice and (B) Ldlr−/−/Par2+/+ and Ldlr−/−/Par2−/− irradiated and repopulated (Par2+/+ or −/− bone marrow) mice. Additionally Ldlr−/−/Par2+/+ and Ldlr−/−/Par2−/− mice, and a cohort of similarly irradiated and repopulated mice, were fed a ‘Western’ diet for 12 (normal and irradiated) and 24 weeks (normal) and their aortic arches (from aortic sinus to end of the subclavian artery) were harvested and processed for (C) mRNA and (D – E) protein examining the chemokines Ccl2 and Cxcl1 (n = 5 each time point and genotype). Histobars represent means ± SEM. * Denotes P < 0.01 for comparisons of −/− to +/+ and −/− recipients to +/+ recipients (ANOVA on ranks with Dunn’s post hoc analysis). Red histobars represent Ldlr−/−/Par2+/+ (and +/+ donors) and blue histobars represent Ldlr−/−/Par2−/− (and −/− donors) mice.

Journal: Arteriosclerosis, thrombosis, and vascular biology

Article Title: Protease-activated Receptor 2 Deficiency Attenuates Atherosclerosis in Mice

doi: 10.1161/ATVBAHA.117.310082

Figure Lengend Snippet: Plasma cytokines were analyzed from aforementioned (A) 12 and 24 week ‘Western’ diet fed Ldlr−/−/Par2+/+ and Ldlr−/−/Par2−/− mice and (B) Ldlr−/−/Par2+/+ and Ldlr−/−/Par2−/− irradiated and repopulated (Par2+/+ or −/− bone marrow) mice. Additionally Ldlr−/−/Par2+/+ and Ldlr−/−/Par2−/− mice, and a cohort of similarly irradiated and repopulated mice, were fed a ‘Western’ diet for 12 (normal and irradiated) and 24 weeks (normal) and their aortic arches (from aortic sinus to end of the subclavian artery) were harvested and processed for (C) mRNA and (D – E) protein examining the chemokines Ccl2 and Cxcl1 (n = 5 each time point and genotype). Histobars represent means ± SEM. * Denotes P < 0.01 for comparisons of −/− to +/+ and −/− recipients to +/+ recipients (ANOVA on ranks with Dunn’s post hoc analysis). Red histobars represent Ldlr−/−/Par2+/+ (and +/+ donors) and blue histobars represent Ldlr−/−/Par2−/− (and −/− donors) mice.

Techniques: Clinical Proteomics, Western Blot, Irradiation

Mouse aortic arch VSMCs were treated for (A & C) 4 or (B & D) 24 hrs with PAR2-AP (100 μM), IL-1β (10 ng/mL), Tnfα (100 ng/mL), or the atherogenic ligand oxidized LDL (oxLDL, 50 μg/mL) and mRNA extracted or protein supernatant quantified at respective time points. mRNA was extrapolated to placebo control (LDL, 50 μg/mL). (E) Par2+/+ and Par2−/− mouse VSMCs were treated with placebo control (LDL, 50 μg/mL), IL-1β (10 ng/mL), Tnfα (100 ng/mL), or oxLDL (50 μg/mL) for 24 hours and monocytes were added to a transwell boyden chamber and infiltration/adhesion quantified (n = 6 performed in triplicate). Circles represent individual measurements, diamonds are means ± SEM. * P < 0.001 for comparisons of −/− to +/+ treatment groups; †P < 0.05 −/− treatment versus control (Two way ANOVA Tukey’s post hoc). Red histobars represent Ldlr−/−/Par2+/+ and blue histobars represent Ldlr−/−/Par2−/− mice.

Journal: Arteriosclerosis, thrombosis, and vascular biology

Article Title: Protease-activated Receptor 2 Deficiency Attenuates Atherosclerosis in Mice

doi: 10.1161/ATVBAHA.117.310082

Figure Lengend Snippet: Mouse aortic arch VSMCs were treated for (A & C) 4 or (B & D) 24 hrs with PAR2-AP (100 μM), IL-1β (10 ng/mL), Tnfα (100 ng/mL), or the atherogenic ligand oxidized LDL (oxLDL, 50 μg/mL) and mRNA extracted or protein supernatant quantified at respective time points. mRNA was extrapolated to placebo control (LDL, 50 μg/mL). (E) Par2+/+ and Par2−/− mouse VSMCs were treated with placebo control (LDL, 50 μg/mL), IL-1β (10 ng/mL), Tnfα (100 ng/mL), or oxLDL (50 μg/mL) for 24 hours and monocytes were added to a transwell boyden chamber and infiltration/adhesion quantified (n = 6 performed in triplicate). Circles represent individual measurements, diamonds are means ± SEM. * P < 0.001 for comparisons of −/− to +/+ treatment groups; †P < 0.05 −/− treatment versus control (Two way ANOVA Tukey’s post hoc). Red histobars represent Ldlr−/−/Par2+/+ and blue histobars represent Ldlr−/−/Par2−/− mice.

Techniques: Control

Review

Structured Review

Images

1) Product Images from "Procoagulant Extracellular Vesicles Increase Neuronal Tau expression, Metabolism and Processing Through Tissue Factor and Protease Activated Receptor 2"

Similar Products

Image Search Results