Journal: Acta biochimica et biophysica Sinica

Article Title: TXNIP aggravates cardiac fibrosis and dysfunction after myocardial infarction in mice by enhancing the TGFB1/Smad3 pathway and promoting NLRP3 inflammasome activation.

doi: 10.3724/abbs.2023150

Figure Lengend Snippet: Figure 3. TXNIP promoted post-MI collagen deposition (A,B) Representative picrosirius red staining images of heart sections from each group at 28 days after treatment (A) under a light microscope and (B) under a polarized light microscope. Collagen I showed red/orange birefringence, while Collagen III showed green/whitish birefringence. (C,E,G) Representative immunohistochemical staining images of heart sections from each group at 28 days after treatment. (C) Collagen I deposition. (E) Collagen III deposition, and (G) ACTA2 deposition. (D) Statistical analysis of Collagen I deposition. Data are shown as the mean±SEM, n=3. **P<0.01. (F) Statistical analysis of Collagen III deposition. Data are shown as the mean± SEM, n=3. **P<0.01. (H) Statistical analysis of ACTA2 deposition. Data are shown as the mean±SEM, n=3. *P<0.05, **P<0.01.

Article Snippet: Then, the membrane was incubated with one of the following antibodies at 4°C overnight: rabbit antiCollagen I, ACTA2, CTGF, TXNIP, Smad3, p-Smad3 (Abcam), antiSmad7, NLRP3, ASC, Caspase-1/Cleaved Caspase-1, Mature IL1B, GAPDH (Wanleibio, Shenyang, China), mouse anti-TGFB1 antibody (Santa Cruz Biotechnology, Dallas, USA), and mouse anti-Collagen III antibody (Boster).

Techniques: Staining, Light Microscopy, Immunohistochemical staining

Journal: Acta biochimica et biophysica Sinica

Article Title: TXNIP aggravates cardiac fibrosis and dysfunction after myocardial infarction in mice by enhancing the TGFB1/Smad3 pathway and promoting NLRP3 inflammasome activation.

doi: 10.3724/abbs.2023150

Figure Lengend Snippet: Figure 4. TXNIP increased post-MI collagen deposition (A) Representative images of the protein levels of Collagen III, Collagen I, ACTA2, and CTGF. (B‒E) Statistical analyses of the protein levels of Collagen I, Collagen III, ACTA2, and CTGF. Data are shown as the mean±SEM, n=3‒5. *P<0.05, **P<0.01; ns, not significant.

Article Snippet: Then, the membrane was incubated with one of the following antibodies at 4°C overnight: rabbit antiCollagen I, ACTA2, CTGF, TXNIP, Smad3, p-Smad3 (Abcam), antiSmad7, NLRP3, ASC, Caspase-1/Cleaved Caspase-1, Mature IL1B, GAPDH (Wanleibio, Shenyang, China), mouse anti-TGFB1 antibody (Santa Cruz Biotechnology, Dallas, USA), and mouse anti-Collagen III antibody (Boster).

Techniques:

Journal: Oncology Letters

Article Title: Estrogen receptor-α36-mediated rapid estrogen signaling regulates 78 kDa glucose-regulated protein expression in gastric carcinoma cells

doi: 10.3892/ol.2018.8542

Figure Lengend Snippet: GRP78 and ER-α36 expression in specimens of human gastric adenocarcinoma. The levels of GRP78 and ER-α36 expression in tumor tissues, adjacent nonmalignant tissues, and corresponding normal tissues were assessed using western blotting. GRP78, 78 kDa glucose-regulated protein; ER-α36, estrogen receptor-α36; T, tumor tissue; A, non-malignant tissue; N, normal tissue.

Article Snippet: Rabbit anti-ER-α36 antibody was provided by the Shenogen Pharma Group Ltd. (Beijing, China).

Techniques: Expressing, Western Blot

Journal: Oncology Letters

Article Title: Estrogen receptor-α36-mediated rapid estrogen signaling regulates 78 kDa glucose-regulated protein expression in gastric carcinoma cells

doi: 10.3892/ol.2018.8542

Figure Lengend Snippet: Associations between GRP78 expression, clinicopathological features of gastric carcinomas and ER-α36 expression.

Article Snippet: Rabbit anti-ER-α36 antibody was provided by the Shenogen Pharma Group Ltd. (Beijing, China).

Techniques: Expressing

Journal: Oncology Letters

Article Title: Estrogen receptor-α36-mediated rapid estrogen signaling regulates 78 kDa glucose-regulated protein expression in gastric carcinoma cells

doi: 10.3892/ol.2018.8542

Figure Lengend Snippet: E2 treatment increases GRP78 and ER-α36 expression and the level of phosphorylated GSK-3β at Ser9 in human gastric adenocarcinoma SGC-7901 cells. Cells were treated with 10−10 M E2 for 24 h and same concentration of alcohol was used for the control group. GRP78 and ER-α36 expression, as well as levels of GSK-3β phosphorylation at Ser9 were measured by (A) western blotting and (B) quantitative analysis of these blots. n=3, **P<0.01 vs. control. E2, 17β-estradiol; GRP78, 78 kDa glucose-regulated protein; ER-α36, estrogen receptor-α36; GSK-3β, glycogen synthase kinase 3β.

Article Snippet: Rabbit anti-ER-α36 antibody was provided by the Shenogen Pharma Group Ltd. (Beijing, China).

Techniques: Expressing, Concentration Assay, Western Blot

Journal: Oncology Letters

Article Title: Estrogen receptor-α36-mediated rapid estrogen signaling regulates 78 kDa glucose-regulated protein expression in gastric carcinoma cells

doi: 10.3892/ol.2018.8542

Figure Lengend Snippet: ER-α36 regulates GRP78 expression and GSK-3β phosphorylation. GRP78 expression and GSK-3β activity were assessed by (A) western blotting and (B) quantitative analysis in SGC-7901 cells with ER-α36-knockdown, cells with forced expression of ER-α36, and control cells transfected with an empty vector. n=3, **P<0.01 vs. SGC-7901. GRP78, 78 kDa glucose-regulated protein; ER-α36, estrogen receptor-α36; GSK-3β, glycogen synthase kinase 3β; 7901-Low36, ER-α36-knockdown SGC-7901 cells; 7901-High36, ER-α36-overexpressing SGC-7901 cells.

Article Snippet: Rabbit anti-ER-α36 antibody was provided by the Shenogen Pharma Group Ltd. (Beijing, China).

Techniques: Expressing, Activity Assay, Western Blot, Transfection, Plasmid Preparation