primary antibodies against collagen i  (Proteintech)

Journal: World Journal of Gastroenterology

Article Title: Evaluation of a 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet-induced mouse model in a comparative experimental study of portal hypertension

doi: 10.3748/wjg.v32.i9.114207

Figure Lengend Snippet: The 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet mouse model (4 weeks) exhibited moderate biliary fibrosis in the portal vein region. A: Hematoxylin-eosin, Masson, and Sirius red staining of mouse livers; B-G: Statistical analysis of Masson and Sirius red staining results; H: Immunohistochemistry staining for collagen-1, α-smooth muscle actin (SMA), and desmin in mouse livers; I-Q: Statistical analysis of collagen-1, α-SMA, and desmin staining results. Sample sizes ( n ): 8:8 (normal chow diet vs 3,5-diethoxycarbonyl-1,4-dihydrocollidine), 8:7 (sham vs bile duct ligation), and 8:7:8 (oil vs 8-week carbon tetrachloride vs 12-week carbon tetrachloride). a P < 0.05. b P < 0.01. c P < 0.001. NS: No significant; NCD: Normal chow diet; DDC: 3,5-diethoxycarbonyl-1,4-dihydrocollidine; BDL: Bile duct ligation; CCl 4 : Carbon tetrachloride; HE: Hematoxylin-eosin; COL1: Collagen-1; SMA: Smooth muscle actin.

Article Snippet: Primary antibodies against collagen 1 (1:2500, catalog No. 67288-1-Ig, Proteintech), α-smooth muscle actin (SMA) (1:200, catalog No. ab5694, Abcam), desmin (1:4000, catalog No. 16520-1-AP, Proteintech), lymphatic vessel endothelial hyaluronan receptor 1 (LyVE-1) (1:100, catalog No. ab219556, Abcam), cluster of differentiation (CD) 34 (1:1000, catalog No. 14486-1-AP, Proteintech), von Willebrand factor (vWF) (1:200, catalog No. 27186-1-AP, Proteintech), vascular endothelial growth factor receptor 2 (VEGFR2) (1:150, catalog No. ab2349, Abcam), vascular endothelial growth factor A (VEGF-A) (1:100, catalog No. ab52917, Abcam), and CD31 (1:5000, catalog No. 11265-1-AP, Proteintech) were applied overnight at 4 °C, followed by 60-minute incubation with secondary antibodies at room temperature.

Techniques: Staining, Immunohistochemistry, Ligation

Journal: Reviews in Cardiovascular Medicine

Article Title: Targeting Tumor Necrosis Factor-α Mitigates Glucose Fluctuation-Induced Aortic Valve Fibrosis: Insights From Diabetic Rat Models

doi: 10.31083/RCM42804

Figure Lengend Snippet: Inhibition of TNF- α mitigates glucose fluctuations-induced aortic valve fibrosis . (A,B,D,E) Immunohistochemical staining for collagen 1 and 3 (indicated by arrows) demonstrated enhanced collagen deposition in the aortic valves of the HG and GF diabetic rat models. However, treatment with infliximab was observed to mitigate this collagen accumulation. (C,F) Immunohistochemical analysis for α -SMA (arrows) revealed an increased fibrotic response in the aortic valves of the diabetic rats in the HG and GF groups; however, infliximab treatment reduced this progression (n = 5 per group). The data are presented as the mean ± SEM. Statistical analyses were conducted utilizing one-way ANOVA, followed by post hoc corrections to account for multiple comparisons (Fig. D–F). * p < 0.05, scale bar = 50 µm or 100 µm. α -SMA, α -smooth muscle actin.

Article Snippet: Additionally, primary polyclonal rabbit antibodies against collagen 1 (14695-1-AP, Proteintech Group, Inc., Chicago, IL, USA) and collagen 3 (227345-1-AP, Proteintech Group, Inc., Chicago, IL, USA) were procured from Proteintech, USA.

Techniques: Inhibition, Immunohistochemical staining, Staining

Journal: Reviews in Cardiovascular Medicine

Article Title: Targeting Tumor Necrosis Factor-α Mitigates Glucose Fluctuation-Induced Aortic Valve Fibrosis: Insights From Diabetic Rat Models

doi: 10.31083/RCM42804

Figure Lengend Snippet: TNF- α -mediated inflammation could exacerbate fibrosis in vitro in porcine aortic valve interstitial cells across different glucose levels . (A,B,E,F) In the primary porcine aortic valve interstitial cells (pAVICs) groups, both HG and GF conditions were found to upregulate collagen 1 protein expression. Moreover, the proinflammatory cytokine TNF- α aggravated this upregulation under HG conditions, with an even more pronounced effect observed under GF conditions. Conversely, the inhibition of TNF- α could reverse these upregulations in both the HG and GF groups. (C,D,G,H) TGF- β 1 protein expression increased under both HG and GF conditions, with TNF- α further enhancing this increase, especially under GF conditions. The inhibition of TNF- α reversed these effects in both groups (n = 4 per group). The data are presented as the mean ± SEM. Statistical analyses were conducted utilizing one-way ANOVA, followed by post hoc corrections to account for multiple comparisons (Fig. E–H). * p < 0.05.

Article Snippet: Additionally, primary polyclonal rabbit antibodies against collagen 1 (14695-1-AP, Proteintech Group, Inc., Chicago, IL, USA) and collagen 3 (227345-1-AP, Proteintech Group, Inc., Chicago, IL, USA) were procured from Proteintech, USA.

Techniques: In Vitro, Expressing, Inhibition