Journal: Journal of the American Society of Nephrology : JASN

Article Title: Specific Macrophage Subtypes Influence the Progression of Rhabdomyolysis-Induced Kidney Injury

doi: 10.1681/ASN.2014040320

Figure Lengend Snippet: The kidney macrophage subtype evolution mirrors kidney function. (A) The elevated BUN levels observed at day 2 (Figure 1F) decreased by day 8, indicating ongoing kidney repair (n=6–11). (B–D) Analysis of macrophages obtained from kidney cell suspensions. Three regions were discriminated according to the expression levels of CD11b and F4/80 as follows: F4/80-CD11b+ (R0), F4/80lowCD11bhigh (R1), and F4/80highCD11b+ (R2). CD11b corresponds to R0+R1+R2 sum. Macrophage distribution among the three regions was affected by glycerol injection at day 2 and day 8. (B) Representative dotplot gated on 30,000 live CD45+ cells. (C) R0, R1, R2, and total CD11b+ cell counts in kidney samples (n=3–5; **P<0.01 and ***P<0.001 compared with day 0; #P<0.05 and ####P<0.0001 compared with day 2). (D) Distribution of CD11b+ cells in the three regions (n=3–5). Macrophage subpopulations were characterized by expression of surface markers using flow cytometry. Mean fluorescence intensity (MFI) is reported on the yaxis for the following markers: (E) CD206 (M2 marker) and (F) CD36 (M2 marker). (n=3–9; *A star above a line displays P<0.05; #displays significant difference between R2 at day 2 or day 8 compared with R2 at day 0 [p<0.05]; $displays significant difference between R1 at day 8 compared with R1 at day 2 [p<0.05]. Lines display means±SEM for individual data).

Article Snippet: Specific primary antibodies were incubated on mouse tissue sections for the detection of F4/80 (rat anti-mouse, 1/100, clone BM8, MF48000; Invitrogen, Saint Aubin, France), collagen III (rabbit anti-mouse, BP8014; Acris Antibodies GmbH, Herford, Germany) or fibronectin (rabbit anti-human/mouse, F3648; Sigma-Aldrich, Saint-Quentin Fallavier, France).

Techniques: Expressing, Injection, Flow Cytometry, Fluorescence, Marker

Journal: Journal of the American Society of Nephrology : JASN

Article Title: Specific Macrophage Subtypes Influence the Progression of Rhabdomyolysis-Induced Kidney Injury

doi: 10.1681/ASN.2014040320

Figure Lengend Snippet: CL-mediated macrophage depletion attenuates kidney lesions 2 days after glycerol injection. Mice received EL or lCL in the saline (NaCl) or the glycerol (Gly) condition according to the protocol shown in Figure 6E. (A and B) CL reduced glycerol-induced fibronectin (Original magnification, ×400 in A) and collagen III (Original magnification, ×200 in B) accumulation at the protein level (left panel; n=3–9) and at the mRNA level in the whole kidney (right panel; n=5–6). (C) Hmox1 was upregulated by glycerol treatment and not modified by CL. CL reduced glycerol-induced Ccl2 and Ccl7 mRNA expression (n=5–6). (Versus NaCl EL: ***P<0.001 and ****P<0.0001. Versus glycerol EL: ##P<0.01; ###P<0.001; ####P<0.0001.) (D) CL reduced glycerol-induced lesions on periodic acid-Schiff staining (Original magnification, ×200 in representative examples). (E) CL did not affect rhabdomyolysis intensity (n=4–8).

Article Snippet: Specific primary antibodies were incubated on mouse tissue sections for the detection of F4/80 (rat anti-mouse, 1/100, clone BM8, MF48000; Invitrogen, Saint Aubin, France), collagen III (rabbit anti-mouse, BP8014; Acris Antibodies GmbH, Herford, Germany) or fibronectin (rabbit anti-human/mouse, F3648; Sigma-Aldrich, Saint-Quentin Fallavier, France).

Techniques: Injection, Saline, Modification, Expressing, Staining

Journal: Journal of the American Society of Nephrology : JASN

Article Title: Specific Macrophage Subtypes Influence the Progression of Rhabdomyolysis-Induced Kidney Injury

doi: 10.1681/ASN.2014040320

Figure Lengend Snippet: CL-mediated macrophage depletion attenuates kidney fibrosis. (A–D) One month after rhabdomyolysis. CTL, age-matched control group; Gly, glycerol-treated group; Gly CL, CL-treated mice according to the pre, post, and glycerol CL protocol depicted in Figure ​Figure6C.6C. (A) BUN levels (n=2–6). (B) CD206+ expression was significantly increased in the glycerol CL condition among CD11b+ cells (R0, R1, and R2) (n=5–8). (C) Collagen III and Masson trichrome staining (representative examples are shown). (D) Collagen III deposit quantification (n=5–7). (Versus control: **P<0.01 and ****P<0.0001. Versus Gly: #P<0.05 and ##P<0.01.) (E–H) Seven months after rhabdomyolysis. NaCl EL, glycerol EL, and pre-glycerol early CL refer to mice treated according to the protocol depicted in Figure 6A. (E) BUN levels (n=6–14). (F) Kidney mass indicated global atrophy after glycerol injection. (n=6–14) (G) Collagen III and Masson trichrome staining (representative examples are shown). (H) Collagen III deposits were still significantly increased in the glycerol condition, which was partially prevented by CL (n=6–14). (Versus NaCl EL: *P<0.05 and ****P<0.0001. Versus glycerol: #P<0.05, ##P<0.01, ####P<0.0001.)

Article Snippet: Specific primary antibodies were incubated on mouse tissue sections for the detection of F4/80 (rat anti-mouse, 1/100, clone BM8, MF48000; Invitrogen, Saint Aubin, France), collagen III (rabbit anti-mouse, BP8014; Acris Antibodies GmbH, Herford, Germany) or fibronectin (rabbit anti-human/mouse, F3648; Sigma-Aldrich, Saint-Quentin Fallavier, France).

Techniques: Control, Expressing, Staining, Injection

Journal: Journal of the American Society of Nephrology : JASN

Article Title: Specific Macrophage Subtypes Influence the Progression of Rhabdomyolysis-Induced Kidney Injury

doi: 10.1681/ASN.2014040320

Figure Lengend Snippet: Proposed early mechanisms involved in rhabdomyolysis-induced kidney injury. (1) In response to myoglobin, tubular cells secrete macrophage chemoattractants (Ccl2, Ccl7). (2) In response to these chemoattractants blood monocytes migrate to the renal interstitium. (3) In addition to its effect on tubular cells, myoglobin polarizes these macrophages toward a proinflammatory phenotype. (4) CD11bhighF4/80lowLy6-Bhigh subtype macrophages enhance renal injury by secreting extracellular matrix compounds (fibronectin, collagen III), proinflammatory cytokines (Il1b, Il12p40) and by increasing recruitment of newly generated macrophages (secretion of Ccl2 and Ccl7).

Article Snippet: Specific primary antibodies were incubated on mouse tissue sections for the detection of F4/80 (rat anti-mouse, 1/100, clone BM8, MF48000; Invitrogen, Saint Aubin, France), collagen III (rabbit anti-mouse, BP8014; Acris Antibodies GmbH, Herford, Germany) or fibronectin (rabbit anti-human/mouse, F3648; Sigma-Aldrich, Saint-Quentin Fallavier, France).

Techniques: Generated

Journal: International Journal of Molecular Sciences

Article Title: MicroRNA-10 Family Promotes Renal Fibrosis through the VASH-1/Smad3 Pathway

doi: 10.3390/ijms25105232

Figure Lengend Snippet: Depletion of miR-10a and miR-10b alleviates RF and Smad3 phosphorylation induced by UUO. ( A ) The process of obtaining KO mice through hybridization. ( B ) Genotype identification: comparison of miR-10a and miR-10b gene-deficient mice with WT mice. ( C ) Representative images (superincumbent image scale bars, 50 µm) of kidney sections from the UUO model stained with H&E and Masson, showing day 7 and day 14; sham serves as the control. ( D ) Expression results of Fibronectin, Col-III, and p-Smad3 in Western blot experiments, with β-actin as the control. ( E ) Expression results of Fibronectin and Col-III in RT-qPCR experiments, with β-actin as the control. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

Article Snippet: Louis, MO, USA) via electrophoresis, followed by blocking with 5% BSA at room temperature for 2 h. Primary antibodies for each protein were diluted in 5% BSA as follows: Fibronectin (1:1000, 26836S, CST), Col-III (1:1000, 66887S, CST), VASH-1 (1:1000, sc-365541, Santa Cruz), p-Smad3 (1:1000, 9520S, CST), Smad3 (1:1000, 9513S, CST), β-actin (1:1000, #AF7018, Affinity), and EGFP (1:5000, SRP15324, Saier); the secondary antibodies used were anti-rabbit (1:40,000, S0001, Affinity) and anti-mouse (1:40,000, S0002, Affinity).

Techniques: Phospho-proteomics, Hybridization, Comparison, Staining, Control, Expressing, Western Blot, Quantitative RT-PCR

Journal: International Journal of Molecular Sciences

Article Title: MicroRNA-10 Family Promotes Renal Fibrosis through the VASH-1/Smad3 Pathway

doi: 10.3390/ijms25105232

Figure Lengend Snippet: Overexpression of miR-10 promotes TGF-β1-induced fibrosis and Smad3 phosphorylation in HK-2 cells. ( A ) Morphological changes in HK-2 cells under 20 ng/mL TGF-β1 stimulation. ( B ) Western blot analysis of Fibronectin, Col-III, and p-Smad3 expression in HK-2 cells under TGF-β1 stimulation, with β-actin as a control. ( C ) RT-qPCR analysis of miR-10a, miR-10b, Fibronectin, and Col-III expression in HK-2 cells under TGF-β1 stimulation, with β-actin as a control. ( D ) Western blot examination of relevant target molecules in HK-2 cells transfected with the corresponding plasmids under TGF-β1 stimulation. * p < 0.05, ** p < 0.01, and **** p < 0.0001.

Article Snippet: Louis, MO, USA) via electrophoresis, followed by blocking with 5% BSA at room temperature for 2 h. Primary antibodies for each protein were diluted in 5% BSA as follows: Fibronectin (1:1000, 26836S, CST), Col-III (1:1000, 66887S, CST), VASH-1 (1:1000, sc-365541, Santa Cruz), p-Smad3 (1:1000, 9520S, CST), Smad3 (1:1000, 9513S, CST), β-actin (1:1000, #AF7018, Affinity), and EGFP (1:5000, SRP15324, Saier); the secondary antibodies used were anti-rabbit (1:40,000, S0001, Affinity) and anti-mouse (1:40,000, S0002, Affinity).

Techniques: Over Expression, Phospho-proteomics, Western Blot, Expressing, Control, Quantitative RT-PCR, Transfection

Journal: International Journal of Molecular Sciences

Article Title: MicroRNA-10 Family Promotes Renal Fibrosis through the VASH-1/Smad3 Pathway

doi: 10.3390/ijms25105232

Figure Lengend Snippet: MiR-10 family promotes fibrosis by modulating the VASH-1/Smad3 pathway. ( A ) Western blot results of VASH-1 in mouse kidneys, with β-actin as a control. ( B ) After stimulation with 20 ng/mL TGF-β1, Western blot and RT-qPCR were performed to detect VASH-1 expression in HK-2 cells, with β-actin as a control. ( C ) After the transfection of HK-2 cells with overexpression plasmids, the results of Western blot and RT-qPCR experiments on the expression of VASH-1, with β-actin as a control, were determined. ( D ) After the transfection of HK-2 cells with knockdown plasmids, the results of Western blot and RT-qPCR experiments on the expression of VASH-1, with β-actin as a control, were determined. ( E ) Under stimulation with 20 ng/mL TGF-β1, after transfection with VASH-1-related plasmids, the protein expression results of Fibronectin, Col-III, and p-Smad3 in HK-2 cells, with β-actin as a control, were determined. ( F ) Under stimulation with 20 ng/mL TGF-β1, after transfection with relevant plasmids, the protein expression results of Fibronectin, Col-III, and p-Smad3 in HK-2 cells, with β-actin as a control, were determined. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

Article Snippet: Louis, MO, USA) via electrophoresis, followed by blocking with 5% BSA at room temperature for 2 h. Primary antibodies for each protein were diluted in 5% BSA as follows: Fibronectin (1:1000, 26836S, CST), Col-III (1:1000, 66887S, CST), VASH-1 (1:1000, sc-365541, Santa Cruz), p-Smad3 (1:1000, 9520S, CST), Smad3 (1:1000, 9513S, CST), β-actin (1:1000, #AF7018, Affinity), and EGFP (1:5000, SRP15324, Saier); the secondary antibodies used were anti-rabbit (1:40,000, S0001, Affinity) and anti-mouse (1:40,000, S0002, Affinity).

Techniques: Western Blot, Control, Quantitative RT-PCR, Expressing, Transfection, Over Expression, Knockdown

Journal: Signal Transduction and Targeted Therapy

Article Title: Peroxiredoxin 4 as a switch regulating PTEN/AKT axis in alveolar macrophages activation

doi: 10.1038/s41392-025-02454-x

Figure Lengend Snippet: PRDX4-mediated activation of AMs promotes epithelial and fibroblast transformation. a The expression of PRDX4 and associated inflammatory genes in MH-S, PBMC-m, and AMs cells was assessed following exposure to CS (50 μg/cm²) at 0, 6, 12, and 24 h. This experiment was conducted three times. b The expression of PRDX4 and associated inflammatory genes was evaluated in MH-S, PBMC-m, and AMs cells after transfection with si_NC and si_PRDX4 and subsequent stimulation with CS (50 μg/cm²) for 24 h. The experiment was repeated three times. c The expression levels of PRDX4 and related inflammatory ( TNF-α, IL-1α, IL-1β, IL-6 ) and profibrotic genes ( TGF-β ) were compared in alveolar lavage fluid from healthy miners (Normal, n = 6) and silicosis patients (Silicosis, n = 10). A dot plot on the right illustrates the correlation analysis between PRDX4 and these inflammatory genes, with each dot representing an individual patient. d A heatmap illustrates the expression of PRDX4 and inflammation-related genes in RNA-sequencing data from lung tissues of normal individuals (n = 7) and silicosis patients (n = 10). The original data were log-transformed [log2 (Gene expression +1)] and presented in heatmap format, with green indicating low expression and red indicating high expression. e The expression of Prdx4 , related inflammatory genes ( Tnf-α, Il-1α, Il-1β, IL-6 ), and fibrotic genes ( Tgf-β , α-sma, col1a1, col3a1) in lung tissues of four groups of mice is shown, with each data point representing an individual mouse. The heatmap on the right displays the correlation between Prdx4 and the expression of related inflammatory genes, with red indicating a positive correlation, and includes data from all four groups of mice. f A heatmap presents the expression of peroxiredoxins ( Prdx1, Prdx3, Prdx6 ) and inflammation-related genes in RNA-sequencing data from normal and silicosis mouse lung tissues. Data are presented as mean ± standard error of the mean (Mean ± SEM). Statistical significance was determined using two-tailed unpaired t-tests ( c ), One-Way ANOVA ( a , e ), Multiple t-tests ( b ), and Two-Way ANOVA ( e ). Correlation analysis was performed using Pearson’s test ( c , e ). The gene expression heatmaps ( d , e ) were generated using the “pheatmap” package in R (version 4.0.2). NS not significant; *P ≤ 0.05; **P ≤ 0.01; ***P ≤ 0.001

Article Snippet: The following antibodies were used: PRDX4 (1:1000, ab59542, Abcam), PTEN (1:1000, 9552, CST), β-Actin (1:10,000, AC026, Abclonal), α-SMA (1:1000, 14968, CST), COL1A1 (1:1000, ab138492, Abcam), COL3A1 (1:1000, 30565, CST), E-Cadherin (1:1000, A20798, Abclonal), N-Cadherin (1:500, A3045, Abclonal), Vimentin (1:500, A2584, Abclonal), Phospho-PI3K p85 (1:1000, 4228T, CST), Phospho-Akt (Thr308) (1:1000, 13038T, CST), Phospho-TAK1(Thr184/187) (1:1000, 4508s, CST), Phospho-NF-kB p65 (1:1000, AP0123, ABclonal), Phospho-c-Jun-S73 (1:500, AP0119, ABclonal), HistoneH3 (1:2000, A2348, Abclonal).

Techniques: Activation Assay, Transformation Assay, Expressing, Transfection, RNA Sequencing, Gene Expression, Two Tailed Test, Generated

Journal: Signal Transduction and Targeted Therapy

Article Title: Peroxiredoxin 4 as a switch regulating PTEN/AKT axis in alveolar macrophages activation

doi: 10.1038/s41392-025-02454-x

Figure Lengend Snippet: Inhibition of PRDX4 activity in vivo significantly ameliorates silicosis-induced fibrosis. a A schematic diagram illustrates the construction process of the mouse model, wherein phosphate-buffered saline PBS and CS were administered via nasal instillation post-anesthesia. PBS (50 μL/time) and CS (50 mg, 50 μL/time) were delivered every three days for a period of 42 days. Conoidin A (Con A, 5 mg/kg) was injected intraperitoneally every three days at a volume of 50 μL. CS, a non-toxic and odorless white powder with particle sizes of 5–10 μm, was suspended in PBS to create a milky solution. Con A was prepared as a clear solution containing 10% DMSO, 40% PEG300, 5% Tween-80, and 45% saline. b Lung function data were collected for three groups of mice: PBS (n = 10), CS (n = 10), and CS+Con A (n = 10). Measurements included tidal volume (TV), expiratory flow rate at 50% of tidal volume (EF50), enhanced pause (PENH), minute ventilation (MV), peak inspiratory flow (PIF), and peak expiratory flow (PEF). Each data point corresponds to an individual mouse. c The lung appearance and body weight change line graph for the three groups of mice are presented. Red and yellow dashed boxes highlight the regions of lung tissue damage. d Histological analysis of lung tissue from three groups of mice was conducted using H&E and Masson staining. High-power magnification images of selected areas are presented in the inset, with dashed lines highlighting regions of lung nodules and collagen deposition. The right column displays the statistical analysis of nodule count and collagen content in lung tissue, where each data point corresponds to an individual mouse. e The hydroxyproline (HYP) content in lung tissue was measured across the three groups of mice, with each data point representing an individual mouse. f IF analysis of α-SMA in lung tissue from the three groups of mice is shown. The right column presents the statistical analysis of α-SMA expression. For this analysis, three mice were selected for IF staining, and three fields of view were examined per mouse, with each data point representing a single field of view. g IF analysis of FAM13A in lung tissue from the three groups of mice is depicted. The right column presents the statistical analysis of FAM13A expression, with each data point representing an individual mouse. IF analysis of p65 ( h ) and AKT ( i ) in AMs from the lung tissue of three groups of mice is depicted. High-power magnification images of AMs, delineated by yellow solid lines, are shown in the inset. White dashed lines outline the macrophages, and red arrows indicate p65 expression. The right column presents the relative expression ratio of p65 and AKT proteins in F4/80-positive macrophages. For this analysis, three mice were selected for IF staining, with three fields of view analyzed per mouse, each data point representing a single field of view. j Expression levels of inflammatory genes ( Tnf-α, Il-1α, Il-1β, Il-6 ) and fibrotic genes ( Tgf-β, α-sma, col1a1, col3a1 ) in lung tissue were measured across the three groups of mice, with each data point representing an individual mouse. The experiment was conducted three times. k, l Changes in body weight, HYP content, FAM13A protein expression, and lung function were assessed in mice following AAV-mediated knockdown of PRDX4 (CS+sh_Prdx4) and Con A blockade (CS+Con A). m A schematic diagram illustrates how PRDX4 regulates the PTEN/AKT/NF-κB pathway to activate AMs and advance the progression of silicosis-associated fibrosis. Scale bars: 20 µm ( h, i ), 50 µm ( f, g ), 100 µm ( d ), 1000 µm ( c ). Abbreviations: al, alveoli; br, bronchi. Data are presented as mean ± standard error of the mean (Mean ± SEM). Statistical significance was determined using two-tailed unpaired t-tests ( c, k, l ), One-Way ANOVA ( b, d, e, f, g, h, i ), and Two-Way ANOVA ( j ). NS, not significant; *P ≤ 0.05; **P ≤ 0.01; ***P ≤ 0.001

Article Snippet: The following antibodies were used: PRDX4 (1:1000, ab59542, Abcam), PTEN (1:1000, 9552, CST), β-Actin (1:10,000, AC026, Abclonal), α-SMA (1:1000, 14968, CST), COL1A1 (1:1000, ab138492, Abcam), COL3A1 (1:1000, 30565, CST), E-Cadherin (1:1000, A20798, Abclonal), N-Cadherin (1:500, A3045, Abclonal), Vimentin (1:500, A2584, Abclonal), Phospho-PI3K p85 (1:1000, 4228T, CST), Phospho-Akt (Thr308) (1:1000, 13038T, CST), Phospho-TAK1(Thr184/187) (1:1000, 4508s, CST), Phospho-NF-kB p65 (1:1000, AP0123, ABclonal), Phospho-c-Jun-S73 (1:500, AP0119, ABclonal), HistoneH3 (1:2000, A2348, Abclonal).

Techniques: Inhibition, Activity Assay, In Vivo, Saline, Injection, Staining, Expressing, Knockdown, Two Tailed Test

Journal: Acta pharmacologica Sinica

Article Title: Synthesis of the novel PARP-1 inhibitor AG-690/11026014 and its protective effects on angiotensin II-induced mouse cardiac remodeling.

doi: 10.1038/aps.2016.159

Figure Lengend Snippet: Figure 2. 6014 attenuated the enlargement of the heart size, cardiomyocytes size and prevented the accumulation of collagen. (A) Representative diagram of mice hearts under different treatment. (B) Representative images diagram of H&E staining of cardiomyocytes. (C) Representative images of Masson’s staining of total collagen in tissue sections of heart. (D) Statistical results of HW/BW. (E) Statistical results of LVW/BW. (F) Statistical areas of total collagen production versus areas of whole tissue. Data were expressed as mean±SEM from three independent experiments. **P<0.01 vs Sham. #P<0.05, ##P<0.01 vs Ang II.

Article Snippet: Anti-PARP-1, anticollagen I and anti-collagen III antibodies were provided by Proteintech Group (Chicago, IL, USA).

Techniques: Staining

Journal: Acta pharmacologica Sinica

Article Title: Synthesis of the novel PARP-1 inhibitor AG-690/11026014 and its protective effects on angiotensin II-induced mouse cardiac remodeling.

doi: 10.1038/aps.2016.159

Figure Lengend Snippet: Figure 3. Effects of 6014 on the expression of hypertrophy marker proteins and fibrosis marker proteins. Protein expression of ANF (A), BNP (B), β-MHC (C), FN (D), collagen I (E) and collagen III (F) were measured by Western blot. Data were expressed as mean±SEM from duplicates in three independent experiments. **P<0.01 vs Sham. #P<0.05, ##P<0.01 vs Ang II.

Article Snippet: Anti-PARP-1, anticollagen I and anti-collagen III antibodies were provided by Proteintech Group (Chicago, IL, USA).

Techniques: Expressing, Marker, Western Blot

Journal: Acta pharmacologica Sinica

Article Title: Synthesis of the novel PARP-1 inhibitor AG-690/11026014 and its protective effects on angiotensin II-induced mouse cardiac remodeling.

doi: 10.1038/aps.2016.159

Figure Lengend Snippet: Figure 4. Effects of 6014 on the expression and enzymatic activity of PARP-1. The expression of PARP-1 in nucleus (A) and whole cell (B) as well as PARylated proteins in whole cell (C). Data were expressed as mean±SEM from duplicates in three independent experiments. *P<0.05, **P<0.01 vs Sham. ##P<0.01 vs Ang II.

Article Snippet: Anti-PARP-1, anticollagen I and anti-collagen III antibodies were provided by Proteintech Group (Chicago, IL, USA).

Techniques: Expressing, Activity Assay

Journal: Acta pharmacologica Sinica

Article Title: Synthesis of the novel PARP-1 inhibitor AG-690/11026014 and its protective effects on angiotensin II-induced mouse cardiac remodeling.

doi: 10.1038/aps.2016.159

Figure Lengend Snippet: Figure 6. Effects of 6014 on the regulation and activity of SIRT-1. NAD+ content analysis (A) and SIRT-1 activity (B) were analyzed. Protein expression of SIRT-1 were measured by Western blot (C). The interaction between SIRT-1 and PARP-1 (D) and the PARylation of SIRT-1 (E) were measured by co-IP assay. Data were expressed as mean±SEM from three independent experiments. *P<0.05, **P<0.01 vs Sham. #P<0.05, ##P<0.01 vs Ang II.

Article Snippet: Anti-PARP-1, anticollagen I and anti-collagen III antibodies were provided by Proteintech Group (Chicago, IL, USA).

Techniques: Activity Assay, Expressing, Western Blot, Co-Immunoprecipitation Assay

Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

Article Title: Inhibiting Lysyl Oxidases prevents pathologic cartilage calcification.

doi: 10.1016/j.biopha.2023.116075

Figure Lengend Snippet: Fig. 6. Proposed mechanism based on the observed results. Increased LOX(L) expression and activity promotes cartilage calcification (Anx, Enpp1, Pit1, Pit2, ALP). Both classical LOX(L) role (matrix cross-links) and non-classical roles are involved. The latter encompass: increased chondrocyte hypertrophy (Runx2, COL10), increased fibrosis (Col1, Col3), increased inflammation (IL-6) and increased oxidative stress (ROS). Finally, cartilage calcification can in turn induce increased LOX (L) activity.

Article Snippet: Collagen 1 (COL1) and Collagen 3 (COL3) expression were evaluated using an anti-COL1 rabbit polyclonal antibody (Boster, PA2140–2) and an anti-COL3 rabbit polyclonal antibody (Origene, AP06517PU-N) respectively.

Techniques: Expressing, Activity Assay

Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology

Article Title: LuQi formula attenuates Cardiomyocyte ferroptosis via activating Nrf2/GPX4 signaling axis in heart failure.

doi: 10.1016/j.phymed.2024.155357

Figure Lengend Snippet: Fig. 3. LQF alleviated TAC-induced cardiac fibrosis in vivo. (A) A four-week longitudinal morphology of mice hearts after sham or TAC surgery (n = 5, scale bar = 500 µm). (B, C) Representative images of Sirius red staining and Masson’s trichrome staining in hearts following sham or TAC surgery for 4 weeks (n = 5, scale bar = 20 µm). (D, E) Quantification of the interstitial fibrotic area in mice at 4 weeks after the sham or TAC surgery (n = 5 for each group). (F, G) Quantification of the perivascular fibrotic area in mice at 4 weeks following the sham or TAC surgery (n = 5 for each group). (H~J) Representative WB image and quantitative analysis of cardiac fibrosis-related proteins, including Col I and Col III (n = 3). (Data are presented as mean ± SEM. ***p < 0.001 vs. sham; ****p < 0.0001 vs. sham; #p < 0.05 vs. TAC; ##p < 0.01 vs. TAC; ###p < 0.001 vs. TAC; ####p < 0.0001 vs. TAC. ns, no significant.).

Article Snippet: The primary antibodies comprised SLC7A11 (26,864–1-AP, Proteintech, China); GPX4 (67,763–1-Ig, Proteintech, China); Nrf2 (16,396–1-AP, Proteintech, China); Collagen I (14,695–1-AP, Proteintech, China); Collagen III (63,034, CST, USA); HO-1 (43,966.

Techniques: In Vivo, Staining