Journal: International journal of molecular sciences

Article Title: Accumulation of Renal Fibrosis in Hyperuricemia Rats Is Attributed to the Recruitment of Mast Cells, Activation of the TGF-β1/Smad2/3 Pathway, and Aggravation of Oxidative Stress.

doi: 10.3390/ijms241310839

Figure Lengend Snippet: Figure 1. Effect of administration of uric acid on the release of Ang II from RBL-2H3 cells. (A,B): The viability of RBL-2H3 cells was determined via CCK-8 assay after treatment with various uric acid concentrations for 24 h or 48 h. (C): Toluidine blue staining of RBL-2H3 after treatment with various uric acid concentrations for 24 h or 48 h. Scale bar = 50 µm. (D,E): Ang II levels in each group after treatment with various uric acid concentrations for 24 h or 48 h. Results are shown as mean ± S.D. (n = 4). * p < 0.05, ** p < 0.01 indicate statistically significant differences compared with the control group.

Article Snippet: MedChemExpress (Monmouth Junction, NJ, USA) supplied Angiotensin II human.

Techniques: CCK-8 Assay, Staining, Control

Journal: International journal of molecular sciences

Article Title: Accumulation of Renal Fibrosis in Hyperuricemia Rats Is Attributed to the Recruitment of Mast Cells, Activation of the TGF-β1/Smad2/3 Pathway, and Aggravation of Oxidative Stress.

doi: 10.3390/ijms241310839

Figure Lengend Snippet: Figure 8. Effects of SCG or VAL on renal oxidative stress in hyperuricemic rats. (A–D): Renal GSH level, renal GSH-Px activity, renal GR activity, and renal MDA level in each group. (E): Serum Ang II level in each group. (F,G): The viability of HK-2 cells was determined via CCK-8 assay after treatment with various Ang II concentrations for 24 h or 48 h. (H): Reactive oxygen species (ROS) levels in each group after incubation of HK-2 cells with different concentrations of Ang II for 24 or 48 h (100×). Results are shown as mean ± S.D. (n = 6). * p < 0.05, ** p < 0.01 indicate statistically significant differences compared with the control group. # p < 0.05, ## p < 0.01 indicate statistically significant differences compared with the model group.

Article Snippet: MedChemExpress (Monmouth Junction, NJ, USA) supplied Angiotensin II human.

Techniques: Activity Assay, CCK-8 Assay, Incubation, Control

Journal: Molecular & Cellular Proteomics : MCP

Article Title: Region- and Cell-type–Resolved Multiomic Atlas of the Heart

doi: 10.1016/j.mcpro.2025.100922

Figure Lengend Snippet: The protective role of atRA in heart failure. A , α-Actinin staining was performed to identify NRCMs. Representative images and quantification of cell size of total 30 microscope fields in each group (group1: NRCMs, group2: NRCMs treated with atRA, group3: NRCM stimulated with Ang II, and group4: NRCM stimulated with Ang II then treated with atRA) are shown. B , the boxplot shows the myocyte cross-sectional area in the four groups. The mRNA levels of hypertrophic genes ( Anp, Bnp ) were determined using qRT-PCR. n = 4 biological replicates for each group. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, ns: not significant. C , the cluster heatmaps indicate the expression patterns of two cluster of proteins detected in NRCM under different conditions (Ang II nonstimulate, Ang II stimulated, Ang II stimulated with atRA treatment). The color bar indicates normalized z-scored iBAQ. The top GOBP terms enriched by each cluster are shown on the right . D , representative global heart photographs of four mice are shown (scale bar represents 2 mm). E , the bar plot shows the heart weight/tibia, heart rate, LV ejection fraction, fractional shortening, LV internal dimension at end-diastole, LV internal dimension at end-systole, LV anterior wall thickness at end-diastole, LV posterior wall thickness at end-systole, all measurements are shown as mean ± SEM. n = 7 biological replicates in Sham group and n = 8 biological replicates in TAC group. F , Masson staining showed strong fibrosis in ventricular regions. Scale bars represent 100 μm. G , the mRNA levels of Ctgf, Cola1 , and Col3a1 were determined using qRT-PCR. n = 6 biologically replicates for each group. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, ns: not significant. H , hematoxylin-eosin (H&E, scale bar = 1 mm) staining and wheat germ agglutinin (WGA, scale bar = 30 μm) staining were performed to determine the hypertrophic degree of the hearts. I , the boxplot shows the myocyte cross-sectional area in the four groups. The mRNA levels of hypertrophic genes ( Anp, Bnp ) were determined using qRT-PCR. n = 6 biologically replicates for each group. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, ns: not significant. J , the bar plot indicates the GOBP enriched in the proteins upregulated in TAC group ( orange ) and downregulated in TAC group ( green ), compared with sham oil group. K , the bar plot shows the GOBP enriched by the proteins upregulated in TAC mice treated with atRA ( orange ) and downregulated in TAC mice treated with atRA ( green ), compared with TAC oil group. L , the western blots show the expression patterns of Rxra, Rxrb, and Gapdh in the four groups (group1: WT mice treated with corn oil, group2: TAC mice treated with corn oil, group3: WT mice treated with atRA, Group4: TAC mice treated with atRA). M , The mRNA level of Rxra and Rxrb were determined using qRT-PCR. n = 7 biologically replicates for each group. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001, ns: not significant. N , the hypothetical mechanism of atRA rescuing heart from cardiac hypertrophy. Under physiological conditions, retinol is oxidized to retinaldehyde by either alcohol dehydrogenase or retinol dehydrogenase (RDH), and retinaldehyde is oxidized to RA by aldehyde dehydrogenase (ALDH). RA is then released and taken up by cardiomyocytes and cellular-RA–binding protein (CRABP) facilitates RA to transport to the nucleus where RA can bind the RA receptor (RAR). When mouse is treated with atRA (60 mg/kg/day) for 4 weeks after TAC surgery, cardiac hypertrophy is relieved. The atRA may act through the activation of Rxr family and maintains cardiac function.

Article Snippet: NRCMs were isolated from 1 to 3 days old Sprague-Dawley rats and cultured in Dulbecco's Modified Eagle Medium/Nutrient Mixture F-12 (DMEM/F12) (Invitrogen, 11330032) with 10% fetal bovine serum for 24 h. Then medium was changed into serum-free DMEM/F12 for 24 h. One micromolar of Angiotensin II (MCE, HY- 13948) treated cells individually or treated cells with 1 μM atRA (Sigma, R2625) collectively for 24 h. After 24 h incubation, cardiomyocytes were collected and lysed for further quantitative real-time PCR (qRT-PCR).

Techniques: Staining, Microscopy, Quantitative RT-PCR, Expressing, Western Blot, Binding Assay, Activation Assay

Journal: BMC pulmonary medicine

Article Title: Angiotensin-(1-7) suppresses airway inflammation and airway remodeling via inhibiting ATG5 in allergic asthma.

doi: 10.1186/s12890-023-02719-7

Figure Lengend Snippet: Fig. 1 Effects of Ang-(1–7) on ATG5 protein expression in IL-13-treated BEAS-2B and HBSMC cells. A BEAS-2B and HBSMC cells were treated with different dose (5, 10, 20, 40 µM) of Ang-(1–7) for 24 h. Cell viability was measured via a CCK-8 kit. BEAS-2B and HBSMC cells were treated with 10 ng/mL human IL-13 for 24 h, then treated with different dose (5, 10, 20 µM) of Ang-(1–7) for 24 h. Expression of ATG5 protein in BEAS-2B cells (B) and HBSMC cells (C) was measured by western blotting. *p < 0.05, **p < 0.01. ns: no significance

Article Snippet: The Ang-(1–7) (#HY-12403, MedChemExpress, China) was dissolved in 1% phosphate buffer solution (PBS), and 1% PBS was used as a control.

Techniques: Expressing, CCK-8 Assay, Western Blot

Journal: BMC pulmonary medicine

Article Title: Angiotensin-(1-7) suppresses airway inflammation and airway remodeling via inhibiting ATG5 in allergic asthma.

doi: 10.1186/s12890-023-02719-7

Figure Lengend Snippet: Fig. 2 Ang-(1–7) treatment suppressed the expression of Beclin-1 protein and secretions of IL-25 and IL-33 in the IL-13-treated BEAS-2B cells. BEAS-2B cells were transfected with control siRNA or ATG5 siRNA, and then treated with IL-13 for 24 h. The IL-13-treated cells were treated with 20 µM Ang-(1–7) for 24 h, and the PBS treatment was as a control treatment. A Cell viability in different groups was measured using a CCK-8 kit. B Expression of Beclin-1 protein was measured using Western blotting. C Secretion of IL-25 and IL-33 was measured using ELISA kits. ns: no significance. *p < 0.05, **p < 0.01

Article Snippet: The Ang-(1–7) (#HY-12403, MedChemExpress, China) was dissolved in 1% phosphate buffer solution (PBS), and 1% PBS was used as a control.

Techniques: Expressing, Transfection, Control, CCK-8 Assay, Western Blot, Enzyme-linked Immunosorbent Assay

Journal: BMC pulmonary medicine

Article Title: Angiotensin-(1-7) suppresses airway inflammation and airway remodeling via inhibiting ATG5 in allergic asthma.

doi: 10.1186/s12890-023-02719-7

Figure Lengend Snippet: Fig. 3 Ang-(1–7) treatment suppressed the expression of Beclin-1, TGF-β1 and α-SMA protein in the IL-13-treated HBSMC cells. HBSMC cells were transfected with control siRNA or ATG5 siRNA, and then treated with IL-13 for 24 h. The IL-13-treated cells were treated with 20 µM Ang-(1–7) for 24 h, and the PBS treatment was as a control treatment. A Cell viability was measured using a CCK-8 kit. B Expression of Beclin-1 protein was measured using Western blotting. C Expression of TGF-β1 and α-SMA protein was measured using Western blotting. ns: no significance. *p < 0.05, **p < 0.01

Article Snippet: The Ang-(1–7) (#HY-12403, MedChemExpress, China) was dissolved in 1% phosphate buffer solution (PBS), and 1% PBS was used as a control.

Techniques: Expressing, Transfection, Control, CCK-8 Assay, Western Blot

Journal: BMC pulmonary medicine

Article Title: Angiotensin-(1-7) suppresses airway inflammation and airway remodeling via inhibiting ATG5 in allergic asthma.

doi: 10.1186/s12890-023-02719-7

Figure Lengend Snippet: Fig. 4 Ang-(1–7) suppressed the results of ATG5 overexpression in IL-13-induced BEAS-2B cells. The BEAS-2B cells were transfected with ATG5 cDNA or vector control, and treated with IL-13 for 24 h. The ATG5 cDNA-transfected or vector control-transfected cells were treated with 20 µM Ang-(1–7) treatment. A Expression of Beclin-1 protein was measured using Western blotting. B Secretion of IL-25 and IL-33 was measured using ELISA kits. **p < 0.01

Article Snippet: The Ang-(1–7) (#HY-12403, MedChemExpress, China) was dissolved in 1% phosphate buffer solution (PBS), and 1% PBS was used as a control.

Techniques: Over Expression, Transfection, Plasmid Preparation, Control, Expressing, Western Blot, Enzyme-linked Immunosorbent Assay

Journal: BMC pulmonary medicine

Article Title: Angiotensin-(1-7) suppresses airway inflammation and airway remodeling via inhibiting ATG5 in allergic asthma.

doi: 10.1186/s12890-023-02719-7

Figure Lengend Snippet: Fig. 5 Ang-(1–7) suppressed the results of ATG5 overexpression in IL-13-induced HBSMC cells. The HBSMC cells were transfected with ATG5 cDNA or vector control, and treated with IL-13 for 24 h. The ATG5 cDNA-transfected or vector control-treated cells were treated with 20 µM Ang-(1–7) treatment. A Expression of Beclin-1, TGF-β1 and α-SMA protein was measured using Western blotting. B Relative expression of Beclin-1 protein was normalized by GAPDH. C Relative expression of TGF-β1 protein was normalized by GAPDH. D Relative expression of α-SMA protein was normalized by GAPDH. *p < 0.05, **p < 0.01

Article Snippet: The Ang-(1–7) (#HY-12403, MedChemExpress, China) was dissolved in 1% phosphate buffer solution (PBS), and 1% PBS was used as a control.

Techniques: Over Expression, Transfection, Plasmid Preparation, Control, Expressing, Western Blot

Journal: BMC pulmonary medicine

Article Title: Angiotensin-(1-7) suppresses airway inflammation and airway remodeling via inhibiting ATG5 in allergic asthma.

doi: 10.1186/s12890-023-02719-7

Figure Lengend Snippet: Fig. 6 Ang-(1–7) treatment or ATG5 knockout suppressed airway inflammation in OVA-challenged mice. A The diagram of animal treatments. An allergic asthma model was induced by OVA in WT mice and ATG5.−/− mice. The OVA-induced WT mice were treated with 30 µg/kg/d Ang-(1–7) for 10 days after sensitization at day 8. B Airway resistance to methacholine were measured. C Levels of IL-4, IL-5 and IL-33 in BALFs were measured using ELISA kits. D Observation of pathological changes by H&E staining. Area of inflammatory infiltration in airway was analyzed using ImageJ software. **p < 0.01

Article Snippet: The Ang-(1–7) (#HY-12403, MedChemExpress, China) was dissolved in 1% phosphate buffer solution (PBS), and 1% PBS was used as a control.

Techniques: Knock-Out, Enzyme-linked Immunosorbent Assay, Staining, Software

Journal: BMC pulmonary medicine

Article Title: Angiotensin-(1-7) suppresses airway inflammation and airway remodeling via inhibiting ATG5 in allergic asthma.

doi: 10.1186/s12890-023-02719-7

Figure Lengend Snippet: Fig. 7 Ang-(1–7) treatment or ATG5 knockout suppressed airway remodeling in by OVA-challenged mice. Expression of α-SMA (A) and TGF-β1 (B) in airway was analyzed by immunohistochemical analysis. Expression of results was analyzed by ImageJ software. *p < 0.05, **p < 0.01

Article Snippet: The Ang-(1–7) (#HY-12403, MedChemExpress, China) was dissolved in 1% phosphate buffer solution (PBS), and 1% PBS was used as a control.

Techniques: Knock-Out, Expressing, Immunohistochemical staining, Software

Journal: BMC pulmonary medicine

Article Title: Angiotensin-(1-7) suppresses airway inflammation and airway remodeling via inhibiting ATG5 in allergic asthma.

doi: 10.1186/s12890-023-02719-7

Figure Lengend Snippet: Fig. 8 Ang-(1–7) treatment or ATG5 knockout suppressed airway autophagy in OVA-challenged mice. A Expression of LC3B in airway was evaluated by immunohistochemical analysis. B Expression of Beclin-1 in airway was evaluated by western blotting. *p < 0.05, **p < 0.01

Article Snippet: The Ang-(1–7) (#HY-12403, MedChemExpress, China) was dissolved in 1% phosphate buffer solution (PBS), and 1% PBS was used as a control.

Techniques: Knock-Out, Expressing, Immunohistochemical staining, Western Blot