Journal: International journal of molecular sciences

Article Title: Endothelial Dysfunction and Impaired Wound Healing Following Radiation Combined Skin Wound Injury.

doi: 10.3390/ijms252312498

Figure Lengend Snippet: Figure 5. Effect of RCI on skin tissue endothelial dysfunction markers. Mice were subjected to sham injury, wounds alone, and 9.0 Gy RCI, and skin tissues surrounding the wounds were collected on days 3, 7, and 14 post-injury. Various markers associated with endothelial dysfunction were assessed in skin tissue lysates using ELISA. The markers analyzed include (Panel A) vascular endothelial growth factor (VEGF); (Panel B) Angiopoietin-2 (Ang2); (Panel C) intercellular adhesion molecule 1 (ICAM1); and (Panel D) insulin-like growth factor 1 (IGF1). Data are expressed as mean ± SEM. Significant differences in these markers were observed: * p < 0.05 for Sham vs. Wound/RCI on days 3, 7, and 14 post-injury, determined by one-way ANOVA followed by Dunnett’s multiple comparison test, and # p < 0.05 for Wound vs. RCI at the same time point, determined by two-way ANOVA followed by Sidak’s multiple comparison test. The sample size ranged from N = 3 to 9 per group per time point.

Article Snippet: The kits used were as follows: Mouse VEGF Immunoassay (MMV00-1, R&D Systems, Inc., Minneapolis, MN, USA), Mouse Angiopoietin-1 ELISA Kit (Colorimetric, NBP3-18634, Novus Biologicals, Centennial, CO, USA), Mouse/Rat Angiopoietin-2 Immunoassay (MANG20, R&D Systems, Inc., Minneapolis, MN, USA), Mouse/Rat IGF-I/IGF-1 Immunoassay (MG100, R&D Systems, Inc., Minneapolis, MN, USA), ICAM1 (CD54) Mouse ELISA Kit (ab100688, abcam, Waltham, MA, USA), Mouse TNF-α Immunoassay (MTA00B-1, R&D Systems, Inc., Minneapolis, MN, USA), Mouse CXCL1/KC Immunoassay (MKC00B-1, R&D Systems, Inc., Minneapolis, MN, USA), Bio-Plex ProTM TGF-β 3-plex assay (171W4001M, Bio-Rad Laboratories, Inc., Hercules, CA, USA), Mouse CTGF ELISA Kit (ab289838, abcam, Waltham, CA, USA), and Mouse Fibronectin ELISA Kit (NBP2-60517, Novus Biologicals, Centennial, CO, USA).

Techniques: Enzyme-linked Immunosorbent Assay, Comparison

Journal: International journal of molecular sciences

Article Title: Endothelial Dysfunction and Impaired Wound Healing Following Radiation Combined Skin Wound Injury.

doi: 10.3390/ijms252312498

Figure Lengend Snippet: Figure 7. Effect of RCI on skin tissue levels of connective tissue growth factor (CTGF) and fibronectin. Mice were subjected to sham injury, wounds alone, and 9.0 Gy RCI, and skin tissues surrounding the wounds were collected on days 3, 7, and 14 post-injury. Levels of (Panel A) CTGF and (Panel B) fi- bronectin were measured in tissue lysates by EKISA. Data are expressed as mean ± SEM. Significant differences in these factors were observed: * p < 0.05 for Sham vs. Wound/RCI on days 3, 7, and 14 post-injury, determined by one-way ANOVA followed by Dunnett’s multiple comparison test, and # p < 0.05 for Wound vs. RCI at the same time point, determined by two-way ANOVA followed by Sidak’s multiple comparison test. The sample size ranged from N = 4 to 9 per group per time point.

Article Snippet: The kits used were as follows: Mouse VEGF Immunoassay (MMV00-1, R&D Systems, Inc., Minneapolis, MN, USA), Mouse Angiopoietin-1 ELISA Kit (Colorimetric, NBP3-18634, Novus Biologicals, Centennial, CO, USA), Mouse/Rat Angiopoietin-2 Immunoassay (MANG20, R&D Systems, Inc., Minneapolis, MN, USA), Mouse/Rat IGF-I/IGF-1 Immunoassay (MG100, R&D Systems, Inc., Minneapolis, MN, USA), ICAM1 (CD54) Mouse ELISA Kit (ab100688, abcam, Waltham, MA, USA), Mouse TNF-α Immunoassay (MTA00B-1, R&D Systems, Inc., Minneapolis, MN, USA), Mouse CXCL1/KC Immunoassay (MKC00B-1, R&D Systems, Inc., Minneapolis, MN, USA), Bio-Plex ProTM TGF-β 3-plex assay (171W4001M, Bio-Rad Laboratories, Inc., Hercules, CA, USA), Mouse CTGF ELISA Kit (ab289838, abcam, Waltham, CA, USA), and Mouse Fibronectin ELISA Kit (NBP2-60517, Novus Biologicals, Centennial, CO, USA).

Techniques: Comparison

Journal: Cell Death & Disease

Article Title: Tenomodulin is essential for prevention of adipocyte accumulation and fibrovascular scar formation during early tendon healing

doi: 10.1038/cddis.2017.510

Figure Lengend Snippet: The absence of Tnmd increases erroneous ECM deposition. ( a , b ) Immunofluorescence staining with anti-Tnmd C-terminal antibody showed Tnmd secretion in the ECM of WT Achilles tendon, but not in Tnmd −/− . ( c–h ) Biglycan, Comp and fibronectin protein deposition in the tendon scar, analyzed by fluorescent digital signal quantification, was clearly augmented in Tnmd −/− when compared with WT mice at 8 days postoperatively. ( i–l ) Biglycan and fibronectin protein levels from cell lysates and supernatant were assessed by ELISA and the levels of both proteins were significantly increased in the supernatant and slightly increased in the cell lysates of Tnmd −/− versus WT TSPCs. For quantification in ( b , d , f and h ), statistical significance was calculated using two-tailed non-parametric Mann–Whitney test, n =3 (3 animals per group; each animal represented by 3 tissue sections). For ELISA in ( i , j , k and l ), statistical significance between 2 groups was determined by unpaired Student’s t -test (two-tailed) for two independent experiments with two donors/genotypes. * P <0.05 compared with WT. S, scar; T, tendon ends. Scale bars: 100 μ m

Article Snippet: Secreted biglycan and fibronectin were determined using mouse biglycan and fibronectin ELISA kits (Cloud-Clone Corp, Katy, TX, USA; and Aviva Systems Biology, San Diego, CA, USA; respectively) according to the manufacturer’s instructions.

Techniques: Immunofluorescence, Staining, Enzyme-linked Immunosorbent Assay, Two Tailed Test, MANN-WHITNEY

Journal: Cell Death & Disease

Article Title: Tenomodulin is essential for prevention of adipocyte accumulation and fibrovascular scar formation during early tendon healing

doi: 10.1038/cddis.2017.510

Figure Lengend Snippet: The absence of Tnmd in TSPCs leads to significantly reduced cell migration and proliferation. ( a – d ) In vitro wound healing assays on collagen I and fibronectin showed that Tnmd −/− TSPC scratch closure was significantly slower compared with WT TSPCs. The borders of the scratches are outlined with yellow lines. ( e , f ) Forward migration index (FMI) plots showed that Tnmd −/− TSPCs were indeed less migratory than WT TSPCs. Upper arrows on each type of matrix show the start point while lower arrows the end point of example migratory cells. ( g–l ) Quantification of velocity, accumulated and Euclidean distances further validated Tnmd −/− migratory deficiency. ( m ) During 0, 4, 8 and 12 days of culture cell growth kinetics were estimated by DNA-based CyQUANT assay revealing that the proliferation of Tnmd −/− TSPCs was significantly lower than that of WT TSPCs. For quantification in ( c , d and m ), n =4 independent experiments per group. For quantifications in random migration, n =3 independent experiments per group (total of 70–80 tracks per genotype). Statistical significance was calculated using two-tailed non-parametric Mann–Whitney test. * P <0.05; ** P <0.01; *** P <0.001, compared with WT. Blue arrows, WT TSPCs; d, day; h, hour; Red arrows, Tnmd −/− TSPCs; Scale bars: 200 μ m

Article Snippet: Secreted biglycan and fibronectin were determined using mouse biglycan and fibronectin ELISA kits (Cloud-Clone Corp, Katy, TX, USA; and Aviva Systems Biology, San Diego, CA, USA; respectively) according to the manufacturer’s instructions.

Techniques: Migration, In Vitro, CyQUANT Assay, Two Tailed Test, MANN-WHITNEY

Journal: Frontiers in cardiovascular medicine

Article Title: Immune checkpoint inhibitor therapy increases systemic SDF-1, cardiac DAMPs Fibronectin-EDA, S100/Calgranulin, galectine-3, and NLRP3-MyD88-chemokine pathways.

doi: 10.3389/fcvm.2022.930797

Figure Lengend Snippet: FIGURE 8 Short-term ICI Therapy increases DAMPs, NLRP3 and MyD-88 mediated fibrosis and vascular inflammation. Short-term treatment with immune checkpoint inhibitors (ICIs) induced significant increases in DAMPs, galectine-3, cytokines and chemokines through NLRP3 and MyD88 pathways inducing myocardial hypertrophy, fibrosis and strong vascular inflammation.

Article Snippet: After centrifugation at 4◦C at 1,300 rpm for 10min, the supernatant of the cardiac homogenates were used to quantitative analysis of six biomarkers of cardiac damages and inflammation, such as: myeloid differentiation primary response 88 (MYd-88) expression (through mouse MyD88 ELISA Kit (My Biosource, San Diego, CA, detection range of 78–5,000 pg/ml; sensitivity: 46.9 pg/ml); NOD-, LRR- and pyrin domaincontaining protein 3 (NLRP-3) (through mouse NLRP3 ELISA Kit (OKEH05486, Aviva Systems Biology); Fibronectin-EDA, S100/Calgranulin and Galectine-3 [three DAMPs (quantified in cardiac tissues through selective quantitative assay); twelve cytokines and growth factors (IL-1α, IL-1β, IL-2, IL-4, IL-6, IL10, IL-12, IL17-α, IFN-γ, TNF-α, G-CSF, GM-CSF) through a mouse cytokine Multiplex Assay kit (Qiagen, USA, pg/mg of heart tissue).

Techniques: