Journal: International journal of molecular sciences

Article Title: Finerenone, a Non-Steroidal Mineralocorticoid Receptor Antagonist, Reduces Vascular Injury and Increases Regulatory T-Cells: Studies in Rodents with Diabetic and Neovascular Retinopathy.

doi: 10.3390/ijms24032334

Figure Lengend Snippet: Figure 3. Finerenone reduced VEGF and vascular leakage in (mRen-2)27 after 12 weeks of diabetes. D, diabetic. Veh, vehicle. Per, perindopril. Fin, finerenone. (A) Three-micrometer paraffin sections of retina immunolabeled with VEGF and counterstained with hematoxylin. GCL, ganglion cell layer. IPL, inner plexiform layer. INL, inner nuclear layer. Scale bar = 40 µm. Ganglion cells denoted by single asterisk (*). Glial cells denoted by double asterisks (**). (B) Quantitation of VEGF immunolabeling in the retina. * p < 0.05 to diabetic+vehicle. n = 4 to 5 rats per group. (C) Vitreal levels of albumin (ELISA). * p < 0.05 to non-diabetic and diabetic+vehicle. # p < 0.05 to non-diabetic. n = 7 to 8 rats per group. Values are mean ± SEM.

Article Snippet: Immunohistochemistry for VEGF was performed by incubating three-micrometer paraffin sections with normal donkey serum for 1 h (D9663, Sigma-Aldrich), and then goat anti-rat VEGF (1:500, 564-RV, R&D Systems, Minneapolis, Minnesota, USA) overnight at 4 ◦C.

Techniques: Immunolabeling, Quantitation Assay, Enzyme-linked Immunosorbent Assay

Journal: International journal of molecular sciences

Article Title: Finerenone, a Non-Steroidal Mineralocorticoid Receptor Antagonist, Reduces Vascular Injury and Increases Regulatory T-Cells: Studies in Rodents with Diabetic and Neovascular Retinopathy.

doi: 10.3390/ijms24032334

Figure Lengend Snippet: Figure 5. Finerenone reduced retinal neovascularization, VEGF, and vascular leakage in mice with OIR at postnatal day 18. RA, room air control. Veh, vehicle. Fin, finerenone. (A) Retinal wholemounts labeled with FITC-isolectin to delineate retinal blood vessels in green. Top panels show whole retina. A quadrant of retina (yellow box) is magnified in the lower panel. Scale bar = 500 µm. Asterisks denote vaso-obliteration. Arrows denote neovascularization. (B) Quantitation of retinal neovascularization. * p < 0.05 to OIR+vehicle. n = 5 to 7 mice per group from 2 to 3 liters per group. (C) Retinal VEGF protein levels (ELISA). (D) Retinal VEGF mRNA levels. (E) Retinal vascular leakage (albumin ELISA). ** p < 0.01, **** p < 0.0001 to RA. # p < 0.05, ### p < 0.001 to OIR + vehicle (Kruskal–Wallis test). n = 5 to 8 mice per group from 2 to 3 litters of mice per group. Values are mean ± SEM.

Article Snippet: Immunohistochemistry for VEGF was performed by incubating three-micrometer paraffin sections with normal donkey serum for 1 h (D9663, Sigma-Aldrich), and then goat anti-rat VEGF (1:500, 564-RV, R&D Systems, Minneapolis, Minnesota, USA) overnight at 4 ◦C.

Techniques: Control, Labeling, Quantitation Assay, Enzyme-linked Immunosorbent Assay

Journal: Exploration of BioMat-X

Article Title: Top2b regulates morphological and migratory properties of retinal progenitor cells in vivo and upon transplantable matrix substrates

doi: 10.37349/ebmx.2025.101335

Figure Lengend Snippet: Figure 6. Cultured retinal progenitor cell groups with Top2b overexpression (OE) and knockdown (KD) illustrate altered expression of select chemotactic receptors compared to wildtype cell groups with no Top2b manipulation (WT). Cell groups illustrated significant differences in the expression of selected chemotactic receptors: vascular endothelial growth factor receptor (VEGFR1), fibroblast growth factor receptor (FGFR1), and c-x-c chemokine receptor 4 (CXCR4, receptor for the stromal cell-derived factor 1, SDF-1a, ligand). Statistical significance across the cell groups is denoted by p-value: * < 0.05, ** < 0.01, **** < 0.0001 as via two-way ANOVA tests followed by Dunnett’s post-hoc test

Article Snippet: Approximately 600 μL of each growth factor vascular endothelial growth factor (VEGF; R&D Systems, Minneapolis, MN, USA, 564-RV), fibroblast growth factor-8 (FGF-8; Invitrogen, Carlsbad, CA, USA, PHG0184), and stromal derived factor 1-a (SDF-1a; Sigma Aldrich, St. Louis, MO, USA, SRP3276) was added to the bottom of separate transwell assays.

Techniques: Cell Culture, Over Expression, Knockdown, Expressing, Derivative Assay

Journal: General physiology and biophysics

Article Title: Tripterine emerges as a potential anti-scarring agent in NIH/3T3 cells by repressing ANRIL.

doi: 10.4149/gpb_2019050

Figure Lengend Snippet: Figure 2. Effect of tripterine treatment on growth of NIH/3T3 cells. A. Cell viability of NIH/3T3 cells after tripterine (2–10 μM, treatment for 4 h) administration by cell counting kit-8 assay. B. Migratory NIH/3T3 cells after tripterine (6 μM, treatment for 4 h) by 24-Transwell assay. Protein expression of Cyclin D1 (C), MMP-2 and MMP-9 (D) as well as VEGF and bFGF (E) in NIH/3T3 cells treated with 6 μM tripterine for 4 h assayed by Western blot assay. Data represented means ± SD. ns p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001. TPR, tripterine; CTRL, control; MMP, matrix metallopeptidase; VEGF, vascular endothelial growth factor; bFGF, basic fibroblast growth factor.

Article Snippet: The polyvinylidene difluoride (PVDF) membranes (Millipore, Bedford, MA, USA) carrying protein imprints were blocked with bovine serum albumin (BSA) (Thermo Fisher Scientific) for 1 h at room temperature, followed by co-incubation with primary antibodies against cyclin D1 (ab16663; Abcam, Cambridge, MA, USA; 1:100), MMP2 (87809; Cell Signaling Technology, CST, Danvers, MA, USA; 1:1,000), MMP-9 (ab38898; Abcam; 1:1,000), vascular endothelial growth factor (VEGF) (MAB4931; R&D Systems, Abingdon, UK; 1 μg/ml), basic fibroblast growth factor (bFGF) (NBP1-18579; Novus Biologicals, Colombia, USA; 1:1,000), β-actin (4967; CST; 1:1,000), total-p65 (8242; CST; 1:1,000), phospho (p) Ser536-p65 (3033; CST; 1:1,000), total-inhibitor of nuclear factor kappa-B alpha (IκBα) (4812; CST; 1:1,000), pSer32-IκBα (2859; CST; 1:1,000).

Techniques: Cell Counting, Transwell Assay, Expressing, Western Blot, Control

Journal: General physiology and biophysics

Article Title: Tripterine emerges as a potential anti-scarring agent in NIH/3T3 cells by repressing ANRIL.

doi: 10.4149/gpb_2019050

Figure Lengend Snippet: Figure 4. Effect of tripterine on the growth of ANRIL-overexpressed NIH/3T3 cells. NIH/3T3 cells were transfected with or without ANRIL, empty vector as a negative control, and then treated with 6 μM tripterine for 4 h. A. ANRIL level assayed by qRT-PCR. B. Cell viability evaluated by cell counting kit-8 assay. C. Cyclin D1 protein expression quantified by Western blot method. D. Migration behav iors assessed by 24-Transwell assay. MMPs (MMP-2 and MMP-9; E) as well as VEGF and bFGF (F) examined by Western blot analysis. Data represented means ± SD. * p < 0.05, ** p < 0.01. MMP, matrix metallopeptidase; VEGF, vascular endothelial growth factor; bFGF, basic fibroblast growth factor. For more abbreviations, see Fig. 3.

Article Snippet: The polyvinylidene difluoride (PVDF) membranes (Millipore, Bedford, MA, USA) carrying protein imprints were blocked with bovine serum albumin (BSA) (Thermo Fisher Scientific) for 1 h at room temperature, followed by co-incubation with primary antibodies against cyclin D1 (ab16663; Abcam, Cambridge, MA, USA; 1:100), MMP2 (87809; Cell Signaling Technology, CST, Danvers, MA, USA; 1:1,000), MMP-9 (ab38898; Abcam; 1:1,000), vascular endothelial growth factor (VEGF) (MAB4931; R&D Systems, Abingdon, UK; 1 μg/ml), basic fibroblast growth factor (bFGF) (NBP1-18579; Novus Biologicals, Colombia, USA; 1:1,000), β-actin (4967; CST; 1:1,000), total-p65 (8242; CST; 1:1,000), phospho (p) Ser536-p65 (3033; CST; 1:1,000), total-inhibitor of nuclear factor kappa-B alpha (IκBα) (4812; CST; 1:1,000), pSer32-IκBα (2859; CST; 1:1,000).

Techniques: Transfection, Plasmid Preparation, Negative Control, Quantitative RT-PCR, Cell Counting, Expressing, Western Blot, Migration, Transwell Assay