cox 2  (Cell Signaling Technology Inc)

Journal: Genes & Diseases

Article Title: Role of miR-101a in targeting Cox-2 to attenuate chondrocyte hypertrophic differentiation and osteoarthritis progression

doi: 10.1016/j.gendis.2025.101839

Figure Lengend Snippet: Bioinformatics prediction of interactions between microRNAs and target genes. (A, B) The Venn diagram displaying miR-101a-3p computationally predicted to target Col10a1 and Cox- 2 by four different prediction algorithms: TargetScan, PicTar, miRDB, and miRCODE. The structure of the predicted duplex by PicTar was shown. (C) TargetScan bioinformatics prediction result of Col10al and Ptgs2 ( Cox-2 ) was performed. (D) miRanda Bioinformatics prediction result of Col10a1 and Ptgs2 ( Cox-2 ).

Article Snippet: The primary antibodies included COL10A1 (ab182563, Abcam, Massachusetts, USA), COX-2 (D223097, Biotechnology, Shanghai, China), MMP13 (ab51072, Abcam, Cambridge, Massachusetts, USA), RUNX2 (#12556, CST, USA), and SOX9 (#82630, CST, USA), which were prepared with primary antibody dilution (Yeasen Biotechnology, China). β-ACTIN was used as an internal control.

Techniques:

Journal: Genes & Diseases

Article Title: Role of miR-101a in targeting Cox-2 to attenuate chondrocyte hypertrophic differentiation and osteoarthritis progression

doi: 10.1016/j.gendis.2025.101839

Figure Lengend Snippet: Col10a1 , Cox-2 , and miR-101a expression in cell lines of chondrocyte hypertrophy. (A) The levels of Col10a1 , Cox-2, and miR-101a were analyzed in proliferative (32 °C) and hypertrophic (37 °C) MCT cells. The expression levels of Col10a1 and Cox-2 significantly increased compared with proliferative MCT cells, whereas miR-101a exhibited weak expression during chondrocyte hypertrophy. (B) The expression levels of Col10a1 , Cox-2 , and miR-101 were shown in the ATDC5 cell line. Both Col10a1 and Cox-2 levels were up-regulated during 21-day 1% ITS induction. However, miR-101 had lower expression in chondrocyte hypertrophy. ∗ P < 0.05 and ∗∗ P < 0.01.

Article Snippet: The primary antibodies included COL10A1 (ab182563, Abcam, Massachusetts, USA), COX-2 (D223097, Biotechnology, Shanghai, China), MMP13 (ab51072, Abcam, Cambridge, Massachusetts, USA), RUNX2 (#12556, CST, USA), and SOX9 (#82630, CST, USA), which were prepared with primary antibody dilution (Yeasen Biotechnology, China). β-ACTIN was used as an internal control.

Techniques: Expressing

Journal: Genes & Diseases

Article Title: Role of miR-101a in targeting Cox-2 to attenuate chondrocyte hypertrophic differentiation and osteoarthritis progression

doi: 10.1016/j.gendis.2025.101839

Figure Lengend Snippet: miR-101a inhibits hypertrophic differentiation of chondrocytes in vitro . (A – C) Relative mRNA levels of Col10a1 , Cox-2 , and Mmp13 after transfected with miR101a mimic in ATDC5 cells. (D – F) Relative mRNA levels of Col10a1 , Cox-2 , and Mmp13 after transfected with miR101a mimic in MCT cells. (G) The protein levels of COL10A1, COX-2, and MMP13 after miR-101a interference in MCT cells were investigated by western blotting. (H) The protein levels of COL10A1, COX-2, and MMP13 after miR-101a interference in hypertrophy-induced ATDC5 cells were detected by western blotting.

Article Snippet: The primary antibodies included COL10A1 (ab182563, Abcam, Massachusetts, USA), COX-2 (D223097, Biotechnology, Shanghai, China), MMP13 (ab51072, Abcam, Cambridge, Massachusetts, USA), RUNX2 (#12556, CST, USA), and SOX9 (#82630, CST, USA), which were prepared with primary antibody dilution (Yeasen Biotechnology, China). β-ACTIN was used as an internal control.

Techniques: In Vitro, Transfection, Western Blot

Journal: Genes & Diseases

Article Title: Role of miR-101a in targeting Cox-2 to attenuate chondrocyte hypertrophic differentiation and osteoarthritis progression

doi: 10.1016/j.gendis.2025.101839

Figure Lengend Snippet: Validation of the targeting effect of miR-101a on Col10a1 and Cox-2. (A) Schematic diagram of the WT and MUT luciferase reporter plasmid constructs. The mutation sequences were generated in the Col10a1 and Cox-2 3′ UTR sequence in the complementary site for the seed region of miR-101a, as indicated. The potential binding sequences are indicated in red, while the sites of mutation are shown in blue. (B) The amplification products of Col10a1 -miR-101a-WT and Col10a1 -miR-101a-MUT were obtained by conventional PCR, and the results of agarose gel electrophoresis showed that the fragment sizes were around 230 bp. (C) Sanger sequencing was utilized to identify the precision of the mutation site on the Col10a1 reporter plasmid. (D) Sanger sequencing was utilized to identify the precision of the mutation site on the Cox-2 reporter plasmid. (E) Luciferase activity of the Col10a1 and Cox-2 3′ UTR reporter was analyzed in 293T cells. ∗ P < 0.05.

Article Snippet: The primary antibodies included COL10A1 (ab182563, Abcam, Massachusetts, USA), COX-2 (D223097, Biotechnology, Shanghai, China), MMP13 (ab51072, Abcam, Cambridge, Massachusetts, USA), RUNX2 (#12556, CST, USA), and SOX9 (#82630, CST, USA), which were prepared with primary antibody dilution (Yeasen Biotechnology, China). β-ACTIN was used as an internal control.

Techniques: Biomarker Discovery, Luciferase, Plasmid Preparation, Construct, Mutagenesis, Generated, Sequencing, Binding Assay, Amplification, Agarose Gel Electrophoresis, Activity Assay

Journal: Genes & Diseases

Article Title: Role of miR-101a in targeting Cox-2 to attenuate chondrocyte hypertrophic differentiation and osteoarthritis progression

doi: 10.1016/j.gendis.2025.101839

Figure Lengend Snippet: Col10a1, COX-2, and miRNA-101a expression after intra-articular injection of miRNA-101 agomir in DMM-induced OA mice. (A – C) The relative mRNA expression levels of miRNA-101 , Col10a1 , and Cox-2 in mouse cartilage at 2, 4, and 6 weeks after intra-articular injection of miRNA-101 agomir ( n = 2 in each group). β-actin and U6 were used as endogenous controls. (D) The immunohistochemical staining of COL10A1 in the articular cartilage tissue of the knee joint. (E) Quantification of the percentage of COL10A1-positive cells in the three groups as determined by the staining results. (F) The immunohistochemical staining of COX-2 in the articular cartilage tissue of the knee joint ( n = 4 in each group). Magnification, 100 × or 400 × . (G) Quantification of the percentage of COX-2 positive cells in the three groups as determined by the staining results. ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001.

Article Snippet: The primary antibodies included COL10A1 (ab182563, Abcam, Massachusetts, USA), COX-2 (D223097, Biotechnology, Shanghai, China), MMP13 (ab51072, Abcam, Cambridge, Massachusetts, USA), RUNX2 (#12556, CST, USA), and SOX9 (#82630, CST, USA), which were prepared with primary antibody dilution (Yeasen Biotechnology, China). β-ACTIN was used as an internal control.

Techniques: Expressing, Injection, Immunohistochemical staining, Staining

Journal: Antioxidants

Article Title: pH-Responsive Cinnamaldehyde–Arginine Nanoprodrug for Targeted Rheumatoid Arthritis Therapy via Antioxidant Activity and Macrophage Reprogramming

doi: 10.3390/antiox15040469

Figure Lengend Snippet: Arg-CA NPs suppress inflammatory responses in vitro. ( A ) Mechanism of Arg-CA NPs in regulating inflammatory signaling pathways in rheumatoid arthritis. Created in BioRender. Yang, S. (2026). https://BioRender.com/m5j27cy (accessed on 10 march 2026). ( B ) Western blot analysis of COX-2, HIF-1α, and NF-κB pathway proteins in RAW264.7 cells after different treatments. ( C – F ) Quantification of protein expression normalized to GAPDH. ( G , H ) ELISA quantification of TNF-α and IL-6 secretion in RAW264.7 cells treated with different groups. Data are presented as mean ± SD ( n = 3). Statistical significance between every 2 groups was calculated via a one-way ANOVA test: ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: Primary antibodies against CD86, CD206, hypoxia-inducible factor-1α (HIF-1α), and cyclooxygenase-2 (COX-2) were purchased from HUABIO (Hangzhou, China), whereas antibodies against p65, phosphorylated p65 (p-p65), phosphorylated IκB-α (p-IκB-α), Arg-1, and iNOS were obtained from ABclonal (Wuhan, China).

Techniques: In Vitro, Protein-Protein interactions, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay