Journal: Bioactive Materials

Article Title: Microenvironment-educated MSC-EVs loaded injectable smart hydrogel for targeting senescent nucleus pulposus cells and inhibiting ferroptosis against intervertebral disc degeneration

doi: 10.1016/j.bioactmat.2026.02.030

Figure Lengend Snippet: D-EVs Alleviate Cellular Senescence and Restore ECM anabolic/catabolic metabolism in Senescent NPCs. (A) The CCK8 assay was used to determine D-EVs concentrations on cell viability. (B) Flow cytometry analysis of proliferative capacity in the above group, and (C) quantitative analysis. (D) Representative ROS images of senescent NPCs treated with N-EVs, D-EVs, or D-EVs + GW4869. (E) Representative SA-β-Gal images of senescent NPCs treated with N-EVs, D-EVs, or D-EVs + GW4869, and (F) quantitative analysis. (G) Confocal analysis of γ-H2A with IF staining depicting DNA damage in the control, TBHP, N-Evs, or D-EVs group. (H) WB analysis of ECM metabolism–related and aging-related proteins in NPCs following treatment with Control, TBHP, N-Evs, or D-EVs. (I) Western blot analysis of p53, p21, and p16 in senescent NPCs treated with D-EVs, D-CM, or D-CM EV-dep . (J) Confocal analysis of COL2 with IF staining in the control, TBHP, N-EVs, or D-EVs group. The data were presented as mean ± SD. n = 3, ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Article Snippet: For immunohistochemistry, the tissue sections were incubated overnight at 4 °C with primary antibodies against COL2 (1:1000, 28459-1-AP, Proteintech) and GPX4 (1:500, 381958, Zen-bio).

Techniques: CCK-8 Assay, Flow Cytometry, Staining, Control, Western Blot

Journal: Bioactive Materials

Article Title: Microenvironment-educated MSC-EVs loaded injectable smart hydrogel for targeting senescent nucleus pulposus cells and inhibiting ferroptosis against intervertebral disc degeneration

doi: 10.1016/j.bioactmat.2026.02.030

Figure Lengend Snippet: Histological evaluation of the D-EVs@Gel ROS in a rat IDD model. (A) Representative histological staining of intervertebral disc tissues (H&E, Safranin O, and Masson) at 4 and 8 weeks post-treatment. Scale bars: 1 mm. (B, E) Immunohistochemical staining and quantification for GPX4, a key inhibitor of ferroptosis, at 4 and 8 weeks post-treatment. (C, F) Immunohistochemical staining and quantification for COL2 at 4 and 8 weeks post-treatment. (D) Quantitative analyses of histological score at 4 and 8 weeks post-treatment. Scale bars: 500 μm. The data were presented as mean ± SD. n = 6, ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Article Snippet: For immunohistochemistry, the tissue sections were incubated overnight at 4 °C with primary antibodies against COL2 (1:1000, 28459-1-AP, Proteintech) and GPX4 (1:500, 381958, Zen-bio).

Techniques: Staining, Immunohistochemical staining

Journal: Bioactive Materials

Article Title: A dual-functional hydrogel integrating adhesive and lubricating interfaces for mitochondrial protection–Driven cartilage regeneration

doi: 10.1016/j.bioactmat.2026.02.051

Figure Lengend Snippet: Regulation of extracellular matrix metabolism by AdHy@Pae in LPS-induced chondrocytes. (A) Representative immunofluorescence images showing the expression of COL2A1, SOX9, MMP9, and ADAMTS5 in different treatment groups and corresponding (B) quantitative analysis. Data are shown as mean ± SD (n = 3, ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001).

Article Snippet: Rat chondrocytes (P1) were seeded in 24-well plates (5 × 10 4 cells per well) and cultured to ∼70–80% confluence, stimulated with LPS (10 μg mL −1 , 12 h) to induce an inflammatory phenotype, and then treated with hydrogel extracts (Hy, AdHy, AdHy@Pae) for 24 h. Cells were washed three times with PBS, fixed in 4% paraformaldehyde for 15 min, permeabilized with 0.1% Triton X-100 (Aladdin, T434386) for 10 min, and blocked with 5% BSA (Solarbio, SW3015) at room temperature for 1 h. Primary antibodies were applied overnight at 4 °C: COL2A1 (Proteintech, 28459-1-AP, 1:200), SOX9 (HUABIO, HA723548, 1:1000), MMP9 (HUABIO, ET1704-69, 1:200), and ADAMTS5 (HUABIO, HA722011, 1:100).

Techniques: Immunofluorescence, Expressing

Journal: Bioactive Materials

Article Title: A dual-functional hydrogel integrating adhesive and lubricating interfaces for mitochondrial protection–Driven cartilage regeneration

doi: 10.1016/j.bioactmat.2026.02.051

Figure Lengend Snippet: Expression analysis of cartilage-related proteins after treatment with AdHy@Pae. (A) Representative Western blot images showing ECM synthesis–related proteins (COL2A1, ACAN, COMP, and SOX9) and antioxidant markers (NRF2 and HO-1) in different groups. (B) Quantitative analysis of matrix-degrading enzymes (MMP13, ADAMTS5, ADAMTS1) and apoptosis-related proteins (BCL-2, Bax, and Caspase-3). Data are presented as mean ± SD (n = 3; ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001).

Article Snippet: Rat chondrocytes (P1) were seeded in 24-well plates (5 × 10 4 cells per well) and cultured to ∼70–80% confluence, stimulated with LPS (10 μg mL −1 , 12 h) to induce an inflammatory phenotype, and then treated with hydrogel extracts (Hy, AdHy, AdHy@Pae) for 24 h. Cells were washed three times with PBS, fixed in 4% paraformaldehyde for 15 min, permeabilized with 0.1% Triton X-100 (Aladdin, T434386) for 10 min, and blocked with 5% BSA (Solarbio, SW3015) at room temperature for 1 h. Primary antibodies were applied overnight at 4 °C: COL2A1 (Proteintech, 28459-1-AP, 1:200), SOX9 (HUABIO, HA723548, 1:1000), MMP9 (HUABIO, ET1704-69, 1:200), and ADAMTS5 (HUABIO, HA722011, 1:100).

Techniques: Expressing, Western Blot

Journal: Bioactive Materials

Article Title: A dual-functional hydrogel integrating adhesive and lubricating interfaces for mitochondrial protection–Driven cartilage regeneration

doi: 10.1016/j.bioactmat.2026.02.051

Figure Lengend Snippet: In vivo validation of the chondroprotective and mitochondrial regulatory effects of AdHy@Pae after therapy for 4 weeks. (A) Representative immunohistochemical staining of cartilage sections for COL2A1, SOX9, MMP3, and ADAMTS1 in different groups (Sham, PBS, Hy, AdHy, and AdHy@Pae). (B) Quantitative analysis of the immunohistochemical staining intensity showing relative expression levels of anabolic (COL2A1, SOX9) and catabolic (MMP3, ADAMTS1) markers. (C) TEM images of chondrocytes showing mitochondrial ultrastructure in each group, with high-magnification views (bottom panels) indicating cristae integrity and membrane morphology. Data are presented as mean ± SD (n = 3); ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗P < 0.0001.

Article Snippet: Rat chondrocytes (P1) were seeded in 24-well plates (5 × 10 4 cells per well) and cultured to ∼70–80% confluence, stimulated with LPS (10 μg mL −1 , 12 h) to induce an inflammatory phenotype, and then treated with hydrogel extracts (Hy, AdHy, AdHy@Pae) for 24 h. Cells were washed three times with PBS, fixed in 4% paraformaldehyde for 15 min, permeabilized with 0.1% Triton X-100 (Aladdin, T434386) for 10 min, and blocked with 5% BSA (Solarbio, SW3015) at room temperature for 1 h. Primary antibodies were applied overnight at 4 °C: COL2A1 (Proteintech, 28459-1-AP, 1:200), SOX9 (HUABIO, HA723548, 1:1000), MMP9 (HUABIO, ET1704-69, 1:200), and ADAMTS5 (HUABIO, HA722011, 1:100).

Techniques: In Vivo, Biomarker Discovery, Immunohistochemical staining, Staining, Expressing, Membrane

Journal: Redox Biology

Article Title: SIRT3-mediated deacetylation of FoxM1 prevents pulmonary fibrosis via modulating the activation of pulmonary fibroblasts

doi: 10.1016/j.redox.2026.104108

Figure Lengend Snippet: FoxM1 is highly expressed in fibroblasts of fibrotic lung tissues. (A, B) qPCR (n = 9) and Western blot (n = 6) analysis of the expression of FoxM1 in normal and IPF lung tissues. ∗ P < 0.05. (C) qPCR analysis of the mRNA levels of FoxM1 in the lung tissues from BLM-treated mice. n = 3, ∗ P < 0.05. (D) Western blot analysis of the protein levels of FoxM1, CTHRC1, α-SMA, and Collagen I in the lung tissues from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (E) The Pearson's correlation analysis of COL1A1 expression with FoxM1 expression based on the RNA-seq results of GSE24206 from GEO database. (F) The Pearson's correlation analysis of Ashcroft score with FoxM1 expression in the lung tissues from BLM-treated mice. (G) Representative images of co-immunostaining for α-SMA and FoxM1 in IPF lung tissues. White arrows indicate double-positive cells. (H) Representative images of co-immunostaining for α-SMA and FoxM1 in the lung tissues from BLM-treated mice. White arrows indicate double-positive cells. (I) Western blot analysis of FoxM1 expression in pulmonary fibroblasts isolated from mice subjected to BLM treatment. n = 3, ∗ P < 0.05. (J) Western blot analysis of FoxM1, CTHRC1, α-SMA, and Collagen I expression in pulmonary fibroblasts treated with TGF-β1. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (A, B, I) and one-way ANOVA with Tukey's post-hoc test (C, D, J) were used for statistical analysis.

Article Snippet: The primary antibodies used were: FoxM1, α-SMA, SIRT3 and Lamin B1 (Selleckchem, Houston, USA), Collagen I (Proteintech, Wuhan, China) and GAPDH (ABclonal, Wuhan, China).

Techniques: Western Blot, Expressing, RNA Sequencing, Immunostaining, Isolation

Journal: Redox Biology

Article Title: SIRT3-mediated deacetylation of FoxM1 prevents pulmonary fibrosis via modulating the activation of pulmonary fibroblasts

doi: 10.1016/j.redox.2026.104108

Figure Lengend Snippet: Impairing nuclear translocation of FoxM1 suppresses fibroblast activation and protects mice from bleomycin-induced pulmonary fibrosis. (A) Western blot analysis was performed to assess the nuclear expression levels of FoxM1 in pulmonary fibroblasts isolated from BLM-treated mice. n = 3, ∗ P < 0.05. (B) Western blot analysis of nuclear FoxM1, CTHRC1, α-SMA, and Collagen I expression in TGF-β1-treated pulmonary fibroblasts accompany with or without RCM-1 treatment. n = 3, ∗ P < 0.05. (C, D) EdU assay for the proliferation of TGF-β1-treated pulmonary fibroblasts accompany with or without RCM-1 treatment. n = 3, ∗ P < 0.05. (E) Hematoxylin–eosin (H&E) and masson's trichrome staining for the lung tissues from BLM-treated mice injected with or without RCM-1. (F, G) The ashcroft score (n = 6, ∗ P < 0.05.) and hydroxyproline contents (n = 6, ∗ P < 0.05.) in the lung tissues of BLM-treated mice injected with or without RCM-1. (H) The survival of BLM-treated mice injected with or without RCM-1. n = 18. (I) Western blot analysis of FoxM1, CTHRC1, α-SMA, and Collagen I expression in the lung tissues from BLM-treated mice injected with or without RCM-1. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (A) and one-way ANOVA with Tukey's post-hoc test (B, D, F–I) were used for statistical analysis.

Article Snippet: The primary antibodies used were: FoxM1, α-SMA, SIRT3 and Lamin B1 (Selleckchem, Houston, USA), Collagen I (Proteintech, Wuhan, China) and GAPDH (ABclonal, Wuhan, China).

Techniques: Translocation Assay, Activation Assay, Western Blot, Expressing, Isolation, EdU Assay, Staining, Injection

Journal: Redox Biology

Article Title: SIRT3-mediated deacetylation of FoxM1 prevents pulmonary fibrosis via modulating the activation of pulmonary fibroblasts

doi: 10.1016/j.redox.2026.104108

Figure Lengend Snippet: Acetylation of FoxM1 is required for the activation of pulmonary fibroblasts. (A, B) Western blot analysis of FoxM1 expression in the cytoplasm and nucleus of CHX-treated pulmonary fibroblasts along with or without MG132 treatment at indicated time. n = 3, ∗ P < 0.05. (C) Western blot analysis of FoxM1 expression in CHX-treated pulmonary fibroblasts along with or without TGF-β1 treatment. n = 3, ∗ P < 0.05. (D) Western blot analysis of the acetylation levels of FoxM1 in pulmonary fibroblasts isolated from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (E) Western blot analysis of the acetylation levels of FoxM1 in pulmonary fibroblasts treated with or without TGF-β1. n = 3, ∗ P < 0.05. (F, G) Western blot analysis of FoxM1 acetylation, CTHRC1, α-SMA, and Collagen I expression in pulmonary fibroblasts treated with TSA (50 nM), or NAM (1 mM) for 24 h, or not. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (D, E) and one-way ANOVA with Tukey's post-hoc test (B, C, G) were used for statistical analysis.

Article Snippet: The primary antibodies used were: FoxM1, α-SMA, SIRT3 and Lamin B1 (Selleckchem, Houston, USA), Collagen I (Proteintech, Wuhan, China) and GAPDH (ABclonal, Wuhan, China).

Techniques: Activation Assay, Western Blot, Expressing, Isolation

Journal: Redox Biology

Article Title: SIRT3-mediated deacetylation of FoxM1 prevents pulmonary fibrosis via modulating the activation of pulmonary fibroblasts

doi: 10.1016/j.redox.2026.104108

Figure Lengend Snippet: Sirt3-dependent deacetylation of FoxM1 regulates the stability of FoxM1. (A) The Pearson's correlation analysis of COL1A1 expression with SIRTs expression based on the RNA-seq results of GSE2052 from GEO database. (B) Western blot analysis of SIRT3 expression in the lung tissues from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (C) Western blot analysis of the acetylation levels of FoxM1 in SIRT3 flox/flox mice intratracheally injected with AAV-Cre. n = 3, ∗ P < 0.05. (D) Western blot analysis was performed to assess the acetylation status of FoxM1 in pulmonary fibroblasts following transfection with Sirt3 siRNA (si-Sirt3). n = 3, ∗ P < 0.05. (E) Western blot analysis of FoxM1 expression in CHX-treated pulmonary fibroblasts transfected with or without si-Sirt3. n = 3, ∗ P < 0.05. (F) Western blot analysis of CTHRC1, α-SMA and Collagen I expression in pulmonary fibroblasts transfected with or without si-Sirt3. n = 3, ∗ P < 0.05. (G) EdU assay for the proliferation of pulmonary fibroblasts transfected with or without si-Sirt3. n = 3, ∗ P < 0.05. (H) Western blot analysis of FoxM1 acetylation, CTHRC1, α-SMA, and Collagen I expression in TGF-β1-treated pulmonary fibroblasts transfected with or without LV-Sirt3. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (B-D, F, G) and one-way ANOVA with Tukey's post-hoc test (E, H) were used for statistical analysis.

Article Snippet: The primary antibodies used were: FoxM1, α-SMA, SIRT3 and Lamin B1 (Selleckchem, Houston, USA), Collagen I (Proteintech, Wuhan, China) and GAPDH (ABclonal, Wuhan, China).

Techniques: Expressing, RNA Sequencing, Western Blot, Injection, Transfection, EdU Assay

Journal: Redox Biology

Article Title: SIRT3-mediated deacetylation of FoxM1 prevents pulmonary fibrosis via modulating the activation of pulmonary fibroblasts

doi: 10.1016/j.redox.2026.104108

Figure Lengend Snippet: Sirt3 knockdown accelerates BLM-induced pulmonary fibrosis via activation pulmonary fibroblasts in vivo. (A) Hematoxylin–eosin (H&E) and masson's trichrome staining for the lung tissues from SIRT3 flox/flox mice or BLM-treated SIRT3 flox/flox mice that intratracheally injected with or without AAV-Cre. (B, C) The ashcroft score (n = 6, ∗ P < 0.05.) and the hydroxyproline contents (n = 6, ∗ P < 0.05.) in the lung tissues of mice treated as in A. (D) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in the lung tissues from mice treated as in A n = 3, ∗ P < 0.05. (E) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in pulmonary fibroblasts isolated from mice treated as in A n = 3, ∗ P < 0.05. (F, G) EdU assay for the proliferation of pulmonary fibroblasts isolated from mice treated as in A. All data were presented as the means ± SEM. One-way ANOVA with Tukey's post-hoc test was used for statistical analysis.

Article Snippet: The primary antibodies used were: FoxM1, α-SMA, SIRT3 and Lamin B1 (Selleckchem, Houston, USA), Collagen I (Proteintech, Wuhan, China) and GAPDH (ABclonal, Wuhan, China).

Techniques: Knockdown, Activation Assay, In Vivo, Staining, Injection, Western Blot, Expressing, Isolation, EdU Assay

Journal: Redox Biology

Article Title: SIRT3-mediated deacetylation of FoxM1 prevents pulmonary fibrosis via modulating the activation of pulmonary fibroblasts

doi: 10.1016/j.redox.2026.104108

Figure Lengend Snippet: Nicotinamide riboside protects mice from bleomycin-induced pulmonary fibrosis via activation of SIRT3. (A) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in TGF-β1-treated pulmonary fibroblasts accompany with or without NR treatment. n = 3, ∗ P < 0.05. (B) Cell viability assessment using the CCK-8 assay in pulmonary fibroblasts treated as in A n = 6, ∗ P < 0.05. (C) The survival of BLM-treated mice oral gavaged with or without NR. n = 18. (D) Hematoxylin–eosin (H&E) and masson's trichrome staining for the lung tissues from mice treated as in C. (E) The ashcroft score of mice treated as in C n = 6, ∗ P < 0.05. (F) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in the lung tissues from mice treated as in C n = 3, ∗ P < 0.05. (G) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in pulmonary fibroblasts isolated from the lung tissues of mice treated as in C n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. One-way ANOVA with Tukey's post-hoc test was used for statistical analysis.

Article Snippet: The primary antibodies used were: FoxM1, α-SMA, SIRT3 and Lamin B1 (Selleckchem, Houston, USA), Collagen I (Proteintech, Wuhan, China) and GAPDH (ABclonal, Wuhan, China).

Techniques: Activation Assay, Western Blot, Expressing, CCK-8 Assay, Staining, Isolation

Journal: International Journal of Molecular Medicine

Article Title: Orcinol glucoside ameliorates pulmonary fibrosis by suppressing hyaluronic acid synthesis and macrophage M2 polarization via targeting hyaluronic acid synthase 2

doi: 10.3892/ijmm.2026.5764

Figure Lengend Snippet: Elevated HAS2 expression and HA accumulation in murine and cellular fibrosis models. (A) Schematic of the experimental design for the time-course study. C57BL/6J mice received a single intratracheal dose of BLM or saline and were sacrificed at the indicated time points (days 0, 3, 5, 7, 10, 14 and 21) for sample collection (n=5 for per group). (B) Representative western blot images (left panel) and densitometric quantification (right panel) showing the protein expression levels of COL1A1 and HAS2 in lung tissues across the time course. β-tubulin served as the loading control (n=4 for per group). (C) ELISA quantification of HA levels in BALF at different days post-BLM injury (n=5 for per group). (D) Schematic diagram illustrating the workflow for the isolation and culture of primary mouse lung fibroblasts from BLM-treated fibrotic mice. (E) Western blotting analysis of HAS2 and COL1A1 protein expression in primary lung fibroblasts isolated from control (saline) and BLM-induced fibrotic mice. Representative blot images (left panel) and densitometric quantification of protein levels normalized to β-tubulin are shown (n=3 for each group). (F) Schematic diagram depicting TGF-β1-induced transition of NIH/3T3 fibroblasts into myofibroblasts. (G) COL1A1, ACTA2, and HAS2 mRNA expression in NIH/3T3 cells was detected using PCR after 5 ng/ml TGF-β1 administration for 12 h (n=3-4 for each group). (H) HAS2 protein expression in NIH/3T3 was detected using western blotting after 5 ng/ml TGF-β1 administration for 24 h (n=3 for each group). (I) ELISA was used to quantify HA concentrations in the culture media of myofibroblasts (n=6 for each group). * P<0.05, ** P<0.01, *** P<0.001. HAS2, hyaluronic acid synthase 2; HA, hyaluronic acid; BLM, bleomycin; BALF, bronchoalveolar lavage fluid; COL1A1, Collagen type I α 1 chain; ACTA2, actin alpha 2, smooth muscle.

Article Snippet: Antibodies for Collagen type I α 1 chain (COL1A1; cat. no. 72026; 1:1,000), Phospho-STAT6 (Tyr641; cat. no. 56554S; 1:1,000) and α-smooth muscle actin (α-SMA; cat. no. 19245; 1:1,000) were obtained from Cell Signaling Technology, Inc.

Techniques: Expressing, Saline, Western Blot, Control, Enzyme-linked Immunosorbent Assay, Isolation

Journal: International Journal of Molecular Medicine

Article Title: Orcinol glucoside ameliorates pulmonary fibrosis by suppressing hyaluronic acid synthesis and macrophage M2 polarization via targeting hyaluronic acid synthase 2

doi: 10.3892/ijmm.2026.5764

Figure Lengend Snippet: OG exerts an anti-pulmonary fibrosis effect by impairing myofibroblast-mediated macrophage M2 polarization. (A) Schematic workflow: Fibroblast treatment with OG during TGF-β1 stimulation, followed by conditioned medium collection and macrophage culture for downstream assays. (B) TGF-β1 release from macrophages measured by ELISA (n=3 for each group). (C) Flow cytometric analysis of CD206 and CD86 expression in macrophages cultured in conditioned medium. The bar graph quantifies the proportion of CD206 + CD86 − cells (M2-like macrophage subpopulation; n=3 for each group). (D) Animal experimental protocol. (E) A BLM-induced mouse model was established to assess the anti-fibrotic effects of OG. Histopathological alterations in lung tissues from different groups were assessed using H&E and Masson's trichrome staining. Scale bars: 500 μ m; magnification, ×40. (F) Western blotting analysis to measure the expression levels of fibrotic markers, COL1A1 and α-SMA, in lung tissues (n=4 for each group). (G) The levels of HA in mouse serum were quantified by ELISA. (H) The levels of TGF-β1 in mouse serum were quantified by ELISA (n=6 for each group). (I) OG concentrations in serum and lung tissues after 14-day oral administration. Left: serum concentrations of OG across treatment groups. Right: lung tissue concentrations of OG, expressed as a percentage of tissue weight (n=3 for each group). * P<0.05, ** P<0.01, *** P<0.001. OG, glucoside; BLM, bleomycin; COL1A1, Collagen type I α 1 chain; α-SMA, α-smooth muscle actin; H&E, hematoxylin and eosin.

Article Snippet: Antibodies for Collagen type I α 1 chain (COL1A1; cat. no. 72026; 1:1,000), Phospho-STAT6 (Tyr641; cat. no. 56554S; 1:1,000) and α-smooth muscle actin (α-SMA; cat. no. 19245; 1:1,000) were obtained from Cell Signaling Technology, Inc.

Techniques: Enzyme-linked Immunosorbent Assay, Expressing, Cell Culture, Staining, Western Blot