Journal: The Journal of Clinical Investigation

Article Title: ADAMTS7 promotes smooth muscle foam cell expansion in atherosclerosis

doi: 10.1172/JCI187451

Figure Lengend Snippet: ( A ) Schematic outlining experimental design and the generation of the SMC transgenic ADAMTS7 mouse. Created with BioRender.com. ( B ) ORO staining of the en face aorta and quantification of lesion area. n = 9. ( C ) Representative images of H&E-stained aortic root sections, quantification of plaque areas ( n = 6). Scale bar: 500 μm. ( D ) Representative images of H&E-stained aortic root sections with necrotic core outlined in dotted line ( n = 6 mice). Scale bar: 300 μm. ( E ) Representative images of aortic root sections stained against α-SMA (Cy3; red), MAC2 (Alexa Fluor 488 green), and cell nuclei (DAPI blue) with their subsequent quantification relative to lesion area ( n = 6). Scale bar: 300 μm. ( F ) Representative Picrosirius red staining of aortic root lesions with bars indicating fibrous cap thickness and quantification of fibrous cap thickness ( n = 6). Scale bar: 300 μm. ( G ) Schematic outlining experimental design and the generation of the EC transgenic ADAMTS7 mouse. Created with BioRender.com. ( H ) ORO staining of the en face aorta and quantification of lesion area. n = 3–4. ( I ) Representative images of H&E-stained aortic root sections and quantification of plaque areas ( n = 5–6). Scale bar: 500 μm. **** P < 0.0001, * P < 0.05. Statistics were analyzed using a 2-tailed Student’s t test.

Article Snippet: The sections then were stained using the following Abs and dilutions: 1:1,000 α-SMA-Cy3 (MilliporeSigma, C6198) and 1:500 MAC2 (Cedarlane, CL8942AP).

Techniques: Transgenic Assay, Staining

Journal: bioRxiv

Article Title: Resolvin D2/GPR18 signaling enhances monocytic myeloid-derived suppressor cell function to mitigate abdominal aortic aneurysm formation

doi: 10.1101/2024.02.23.581672

Figure Lengend Snippet: RvD2 administration decreases aortic aneurysm phenotype and preserves morphology to mitigate AAA formation. A , Schematic description of murine topical elastase model with RvD2 treatments. Mice were divided into three groups and treated with either heat-inactivated elastase or elastase on day 0. Mice were then administered either vehicle or RvD2. Aortic diameter was measured on day 14 and tissue harvested for additional analysis. B , RvD2 treated mice demonstrated a significant decrease in aortic diameter compared to vehicle treated mice; *p<0.001 vs. other groups; n=10-20 per group). C , Representative images of aortic phenotype in the respective groups. D , Comparative histology performed on day 14 indicates that elastase-treated mice administered with RvD2 have a marked increase in smooth muscle cell α-actin (SM-α actin) expression, decrease in elastic fiber disruption (Verhoeff-Van Gieson staining for elastin) as well as neutrophil (PMN) and macrophage (Mac-2) infiltration, compared to elastase-treated WT mice alone (n=5 per group). Representative histological images in the respective groups with arrows indicate areas of immunostaining. E , Quantification of histological staining in respective groups; n=5 per group; *p<0.02 vs. other groups.

Article Snippet: Slides of aortic cross-sections were prepared and stained for elastin (Van Gieson’s Solution, catalog no. s289; Poly Scientific R&D Systems, Bay Shore, NY) smooth muscle actin (monoclonal anti-actin α-smooth muscle, Sigma Aldrich, St. Louis, MO), macrophages (purified anti-mouse Mac-2, Cedarlane Laboratories, Burlington, Canada), and neutrophils (rat anti-mouse neutrophils, AbD Serotec, Oxford, UK).

Techniques: Expressing, Disruption, Staining, Immunostaining

Journal: bioRxiv

Article Title: Resolvin D2/GPR18 signaling enhances monocytic myeloid-derived suppressor cell function to mitigate abdominal aortic aneurysm formation

doi: 10.1101/2024.02.23.581672

Figure Lengend Snippet: In vivo GPR18 knockdown reduces the protective effect of RvD2. A , GPR18-siRNA treatment of WT mice demonstrated a significant increase in aortic diameter as compared to control (c)-siRNA treated mice after administration of RvD2 in respective groups (*p=0.004, n=12-13 per group). B , Representative images of aortic phenotype in respective groups. C, Expression of smooth muscle-α actin is significantly increased, and elastin fragmentation as well as macrophage and neutrophil infiltration in aortic tissue are significantly decreased in mice treated with c-siRNA+RvD2 compared to mice treated with GPR18 siRNA+RvD2 (n=5 per group). Arrows indicate areas of immunostaining. D, Quantification of histological staining in respective groups; n=5 per group; *p<0.01 vs. other groups.

Article Snippet: Slides of aortic cross-sections were prepared and stained for elastin (Van Gieson’s Solution, catalog no. s289; Poly Scientific R&D Systems, Bay Shore, NY) smooth muscle actin (monoclonal anti-actin α-smooth muscle, Sigma Aldrich, St. Louis, MO), macrophages (purified anti-mouse Mac-2, Cedarlane Laboratories, Burlington, Canada), and neutrophils (rat anti-mouse neutrophils, AbD Serotec, Oxford, UK).

Techniques: In Vivo, Knockdown, Control, Expressing, Immunostaining, Staining