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Proteintech collagen type ii α1

Micro-CT evaluations of AZ-treated OA induced by DMM surgery. (A) Chemical structure of AZ. (B) Nuclear magnetic resonance spectrum of AZ. (C) Micro-CT images of frontal views of the knee joints at 4 weeks after sham or DMM operation. (D) Sagittal views of the medial compartment subchondral bone. Quantitative analysis of (E) BV, (F) BV/TV, (G) Tb. N and (H) Tb. Th. # P<0.05 vs. control; *P<0.05 vs. DMM. AZ, acetyl zingerone; BV, bone volume; DMM, destabilization of the medial meniscus; Tb. N; trabecular number; Tb. Th, trabecular thickness; TV, total volume.

Collagen Type Ii α1, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 584 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/collagen+type+ii+%CE%B11/Collagen+Type+II+Antibody/pmc10540024-134-58-90
Average 96 stars, based on 584 article reviews

collagen type ii α1 - by Bioz Stars, 2026-09

96/100 stars

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1) Product Images from "Acetyl zingerone ameliorates osteoarthritis by inhibiting chondrocyte programmed cell death"

Article Title: Acetyl zingerone ameliorates osteoarthritis by inhibiting chondrocyte programmed cell death

Journal: Molecular Medicine Reports

doi: 10.3892/mmr.2023.13089

Figure Legend Snippet: Micro-CT evaluations of AZ-treated OA induced by DMM surgery. (A) Chemical structure of AZ. (B) Nuclear magnetic resonance spectrum of AZ. (C) Micro-CT images of frontal views of the knee joints at 4 weeks after sham or DMM operation. (D) Sagittal views of the medial compartment subchondral bone. Quantitative analysis of (E) BV, (F) BV/TV, (G) Tb. N and (H) Tb. Th. # P<0.05 vs. control; *P<0.05 vs. DMM. AZ, acetyl zingerone; BV, bone volume; DMM, destabilization of the medial meniscus; Tb. N; trabecular number; Tb. Th, trabecular thickness; TV, total volume.

Techniques Used: Micro-CT, Nuclear Magnetic Resonance, Control

AZ promotes chondrocyte proliferation, and inhibits the expression of inflammatory factors and matrix-degrading enzymes. Chondrocytes were pretreated with DMSO and IL-1β (20 ng/ml) for 24 h, and were then treated with AZ (25, 50 and 100 µM) for another 24 or 48 h. (A) Cell viability was assessed using the Cell Counting Kit-8 assay. (B) EdU staining (red fluorescence) was used to assess cell proliferation. (C) Expression levels of aggrecan and COL2A1. (D) ImageJ was used to analyze the relative protein expression levels of aggrecan, COL2A1, ADAMTS-4, iNOS, MMP13 and COX2. (E) ADAMTS-4, iNOS, MMP13 and COX2 were detected by western blotting. # P<0.05 vs. control; *P<0.05 vs. IL-1β. AZ, acetyl zingerone; COL2A1, collagen type II α1; COX2, cyclooxygenase 2; EdU, 5-ethynyl-2′-deoxyuridine; iNOS, inducible nitric oxide synthase.

Figure Legend Snippet: AZ promotes chondrocyte proliferation, and inhibits the expression of inflammatory factors and matrix-degrading enzymes. Chondrocytes were pretreated with DMSO and IL-1β (20 ng/ml) for 24 h, and were then treated with AZ (25, 50 and 100 µM) for another 24 or 48 h. (A) Cell viability was assessed using the Cell Counting Kit-8 assay. (B) EdU staining (red fluorescence) was used to assess cell proliferation. (C) Expression levels of aggrecan and COL2A1. (D) ImageJ was used to analyze the relative protein expression levels of aggrecan, COL2A1, ADAMTS-4, iNOS, MMP13 and COX2. (E) ADAMTS-4, iNOS, MMP13 and COX2 were detected by western blotting. # P<0.05 vs. control; *P<0.05 vs. IL-1β. AZ, acetyl zingerone; COL2A1, collagen type II α1; COX2, cyclooxygenase 2; EdU, 5-ethynyl-2′-deoxyuridine; iNOS, inducible nitric oxide synthase.

Techniques Used: Expressing, Cell Counting, Staining, Fluorescence, Western Blot, Control

AZ inhibits IL-1β-induced ferroptosis in chondrocytes. (A) GSH and (B) MDA levels were measured in each group using GSH and MDA assays. Chondrocytes were pretreated with IL-1β (20 ng/ml) or Fer-1 (60 nmol/ml) for 24 h and then treated with or without AZ (100 µM) for an additional 24 h. (C) Mitochondria were observed by transmission electron microscopy. (D) GPX4 staining to indicate ferroptosis in mice following DMM surgery. (E) Cells were observed by fluorescence microscopy. (F) Chondrocytes were pretreated with or without IL-1β (20 ng/ml) or Fer-1 (60 nmol/ml) for 24 h and then treated with AZ (100 µM) for another 24 h, and GPX4 expression was determined by western blotting. # P<0.05 vs. control; *P<0.05 vs. IL-1β. AZ, acetyl zingerone; DMM, destabilization of the medial meniscus; Fer-1, ferrostatin-1; GPX4, glutathione peroxidase 4; GSH, glutathione; MDA, malondialdehyde.

Figure Legend Snippet: AZ inhibits IL-1β-induced ferroptosis in chondrocytes. (A) GSH and (B) MDA levels were measured in each group using GSH and MDA assays. Chondrocytes were pretreated with IL-1β (20 ng/ml) or Fer-1 (60 nmol/ml) for 24 h and then treated with or without AZ (100 µM) for an additional 24 h. (C) Mitochondria were observed by transmission electron microscopy. (D) GPX4 staining to indicate ferroptosis in mice following DMM surgery. (E) Cells were observed by fluorescence microscopy. (F) Chondrocytes were pretreated with or without IL-1β (20 ng/ml) or Fer-1 (60 nmol/ml) for 24 h and then treated with AZ (100 µM) for another 24 h, and GPX4 expression was determined by western blotting. # P<0.05 vs. control; *P<0.05 vs. IL-1β. AZ, acetyl zingerone; DMM, destabilization of the medial meniscus; Fer-1, ferrostatin-1; GPX4, glutathione peroxidase 4; GSH, glutathione; MDA, malondialdehyde.

Techniques Used: Transmission Assay, Electron Microscopy, Staining, Fluorescence, Microscopy, Expressing, Western Blot, Control

AZ inhibits ferroptosis in osteoarthritis through the Nrf2/HO-1 pathway. Chondrocytes were pretreated with IL-1β (20 ng/ml) for 24 h, with or without ML385 (Nrf2 inhibitors) or Fer-1 (60 nmol/ml) for 12 h, and then treated with or without AZ (100 µM) for an additional 24 h. (A) Protein expression levels of Nrf2, HO-1 and GPX4 was determined by western blotting. (B) Nrf2 staining of ferroptosis in chondrocytes. Chondrocytes were pretreated with IL-1β (20 ng/ml) for 24 h, with or without tin protoporphyrin IX (HO-1 inhibitors) or Fer-1 (60 nmol/ml) for 12 h, and then treated with or without AZ (100 µM) for an additional 24 h. (C) Protein expression levels of Nrf2, HO-1 and GPX4 was determined by western blotting. (D) Schematic diagram showing how AZ affects ferroptosis through the Nrf2/HO-1 signaling pathway. AZ, acetyl zingerone; DMM, destabilization of the medial meniscus; Fer-1, ferrostatin-1; GPX, glutathione peroxidase 4; HO-1, heme oxygenase-1; Nrf2, nuclear factor erythroid 2-related factor 2.

Figure Legend Snippet: AZ inhibits ferroptosis in osteoarthritis through the Nrf2/HO-1 pathway. Chondrocytes were pretreated with IL-1β (20 ng/ml) for 24 h, with or without ML385 (Nrf2 inhibitors) or Fer-1 (60 nmol/ml) for 12 h, and then treated with or without AZ (100 µM) for an additional 24 h. (A) Protein expression levels of Nrf2, HO-1 and GPX4 was determined by western blotting. (B) Nrf2 staining of ferroptosis in chondrocytes. Chondrocytes were pretreated with IL-1β (20 ng/ml) for 24 h, with or without tin protoporphyrin IX (HO-1 inhibitors) or Fer-1 (60 nmol/ml) for 12 h, and then treated with or without AZ (100 µM) for an additional 24 h. (C) Protein expression levels of Nrf2, HO-1 and GPX4 was determined by western blotting. (D) Schematic diagram showing how AZ affects ferroptosis through the Nrf2/HO-1 signaling pathway. AZ, acetyl zingerone; DMM, destabilization of the medial meniscus; Fer-1, ferrostatin-1; GPX, glutathione peroxidase 4; HO-1, heme oxygenase-1; Nrf2, nuclear factor erythroid 2-related factor 2.

Techniques Used: Expressing, Western Blot, Staining

Image Search Results

NFATc1 expression in IVD. (A) Immunohistochemical analysis of NFATc1 was performed on IVD tissues at different Pfirrmann (PF) grades. Quantification was reported and expressed as % of positive cells per area (3–5 sections per sample; PF I–II group, n = 7; PF III group, n = 6; PF IV–V group, n = 6). * p < 0.001 PF IV–V group vs PF I–II group and PF IV–V group vs PF III. (B) NFATc1 expression was analyzed in IVD cells during the de-differentiation process from P0 to P2 passages by immunocytochemistry, and representative photomicrographs are reported. Protein levels were quantified by densitometric analysis of immunocytochemical pictures using ImageJ software. Quantitative analysis of at least 10 fields per replicate was performed. Protein levels are expressed as fold change relative to P0 cells. Data are presented as the mean ± SD (n = 4). * p < 0.05. Scale bar = 20 μm.

Journal: Frontiers in Cell and Developmental Biology

Article Title: The NFATc1/P2X7 receptor relationship in human intervertebral disc cells

doi: 10.3389/fcell.2024.1368318

Figure Lengend Snippet: NFATc1 expression in IVD. (A) Immunohistochemical analysis of NFATc1 was performed on IVD tissues at different Pfirrmann (PF) grades. Quantification was reported and expressed as % of positive cells per area (3–5 sections per sample; PF I–II group, n = 7; PF III group, n = 6; PF IV–V group, n = 6). * p < 0.001 PF IV–V group vs PF I–II group and PF IV–V group vs PF III. (B) NFATc1 expression was analyzed in IVD cells during the de-differentiation process from P0 to P2 passages by immunocytochemistry, and representative photomicrographs are reported. Protein levels were quantified by densitometric analysis of immunocytochemical pictures using ImageJ software. Quantitative analysis of at least 10 fields per replicate was performed. Protein levels are expressed as fold change relative to P0 cells. Data are presented as the mean ± SD (n = 4). * p < 0.05. Scale bar = 20 μm.

Article Snippet: The primary antibodies against SOX9 (# sc-20095), aggrecan (ACAN, # sc-33695), HIF-1α (H1α67, # sc-53546), NFATc1 (7A6, # sc-7294; H-10, # sc-1783; H-110, # sc-13033), lamin A/C (E-1, # sc-376248), and normal mouse IgG 1 (# sc-3877) were purchased from Santa Cruz Biotechnology, Inc. (Dallas, TX, United States), while anti-collagen type II α1 chain (COL2a1; # ab3092) antibody was purchased from Abcam (Cambridge, United Kingdom), anti-HIF-1α (H1 alpha67, # NB100–134) was purchased from Novus Biologicals (Centennial, CO, United States), anti-P2X7R C-terminal (# APR-004) was purchased from Alomone Labs (Jerusalem, Israel), and anti-P2X7R C-terminal (#P8232) and anti-P2X7R extracellular loop (#P9122) were purchased from Sigma-Aldrich, Merck KGaA (Milan, Italy).

Techniques: Expressing, Immunohistochemical staining, Immunocytochemistry, Software

Overexpression of NFATc1 upregulates P2X7R expression in human IVD cells. IVD cells were transfected with 100 ng or 200 ng of pRSV-NFATc1/A expression vector (NFATc1) for 16 h and treated with PMA (20 nM) and ionomycin (1 μM) for 3 h. Cells were collected and subjected to RNA and protein analysis. mRNA levels of NFATc1 and P2X7R were determined by real-time RT-PCR. RNA relative expression levels were normalized to untreated cells and expressed as fold change. Data represent means ± SD (n = 3). * p < 0.01; ** p < 0.0001. Protein levels of NFATc1 and P2X7R were analyzed by immunocytochemistry, and representative optical photomicrographs of immunostaining are shown. Protein levels were quantified by densitometric analysis of immunocytochemical pictures using ImageJ software. Quantitative analysis of at least 10 fields per replicate was performed. Protein levels are expressed as fold change relative to untreated cells. Data are presented as the mean ± SD (n = 3). * p < 0.05. Scale bar = 20 μm.

Journal: Frontiers in Cell and Developmental Biology

Article Title: The NFATc1/P2X7 receptor relationship in human intervertebral disc cells

doi: 10.3389/fcell.2024.1368318

Figure Lengend Snippet: Overexpression of NFATc1 upregulates P2X7R expression in human IVD cells. IVD cells were transfected with 100 ng or 200 ng of pRSV-NFATc1/A expression vector (NFATc1) for 16 h and treated with PMA (20 nM) and ionomycin (1 μM) for 3 h. Cells were collected and subjected to RNA and protein analysis. mRNA levels of NFATc1 and P2X7R were determined by real-time RT-PCR. RNA relative expression levels were normalized to untreated cells and expressed as fold change. Data represent means ± SD (n = 3). * p < 0.01; ** p < 0.0001. Protein levels of NFATc1 and P2X7R were analyzed by immunocytochemistry, and representative optical photomicrographs of immunostaining are shown. Protein levels were quantified by densitometric analysis of immunocytochemical pictures using ImageJ software. Quantitative analysis of at least 10 fields per replicate was performed. Protein levels are expressed as fold change relative to untreated cells. Data are presented as the mean ± SD (n = 3). * p < 0.05. Scale bar = 20 μm.

Techniques: Over Expression, Expressing, Transfection, Plasmid Preparation, Quantitative RT-PCR, Immunocytochemistry, Immunostaining, Software

In silico analysis of the human P2RX7 gene promoter region (−2000 to +32 bp). Nucleotide numbering is relative to the first nucleotide (adenine +1) of the TSS, which is indicated with an arrow. The positions of putative transcription factor-binding motifs of NFATc1 and HIF-1α identified using the JASPAR database software are boxed.

Journal: Frontiers in Cell and Developmental Biology

Article Title: The NFATc1/P2X7 receptor relationship in human intervertebral disc cells

doi: 10.3389/fcell.2024.1368318

Figure Lengend Snippet: In silico analysis of the human P2RX7 gene promoter region (−2000 to +32 bp). Nucleotide numbering is relative to the first nucleotide (adenine +1) of the TSS, which is indicated with an arrow. The positions of putative transcription factor-binding motifs of NFATc1 and HIF-1α identified using the JASPAR database software are boxed.

Techniques: In Silico, Binding Assay, Software

Journal: Molecular Medicine Reports

Article Title: Acetyl zingerone ameliorates osteoarthritis by inhibiting chondrocyte programmed cell death

doi: 10.3892/mmr.2023.13089

Figure Lengend Snippet: Micro-CT evaluations of AZ-treated OA induced by DMM surgery. (A) Chemical structure of AZ. (B) Nuclear magnetic resonance spectrum of AZ. (C) Micro-CT images of frontal views of the knee joints at 4 weeks after sham or DMM operation. (D) Sagittal views of the medial compartment subchondral bone. Quantitative analysis of (E) BV, (F) BV/TV, (G) Tb. N and (H) Tb. Th. # P<0.05 vs. control; *P<0.05 vs. DMM. AZ, acetyl zingerone; BV, bone volume; DMM, destabilization of the medial meniscus; Tb. N; trabecular number; Tb. Th, trabecular thickness; TV, total volume.

Article Snippet: The following primary and secondary antibodies were used in the present study: Nrf2 (cat. no. 16396-1-AP; 1:2,000), HO-1 (cat. no. 10701-1-AP; 1:1,000), GPX4 (cat. no. 67763-1-lg; 1:2,000), ADAMTS-4 (cat. no. 11865-1-AP; 1:500), inducible nitric oxide synthase (iNOS; cat. no. 18985-1-AP; 1:1,000), MMP13 (cat. no. 18165-1-AP; 1:1,000), cyclooxygenase 2 (COX2; cat. no. 27308-1-AP; 1:1,000), aggrecan (cat. no. 13880-1-AP; 1:1,000), collagen type II α1 (COL2A1; cat. no. 28459-1-AP; 1:1,000), Notch1 (cat. no. 20687-1-AP; 1:1,000), suppressor of cytokine signaling 3 (SOCS3; cat. no. 14025-1-AP; 1:1,000) and β-actin (cat. no. 66009-1-lg; 1:4,000) (all from Proteintech Group Inc.), and caspase 3 (cat. no. A0214; 1:1,000) and cleaved caspase 3 (cat. no. A19654; 1:1,000) (both from ABclonal Biotech Co., Ltd.) primary antibodies; HRP-conjugated AffiniPure goat anti-rabbit IgG (H+L) (cat. no. SA00001-2; 1:8,000) and HRP-conjugated AffiniPure goat anti-mouse IgG (H+L) (cat. no. SA00001-1; 1:8,000) secondary antibodies (both from Proteintech Group Inc.).

Techniques: Micro-CT, Nuclear Magnetic Resonance, Control

Journal: Molecular Medicine Reports

Article Title: Acetyl zingerone ameliorates osteoarthritis by inhibiting chondrocyte programmed cell death

doi: 10.3892/mmr.2023.13089

Figure Lengend Snippet: AZ promotes chondrocyte proliferation, and inhibits the expression of inflammatory factors and matrix-degrading enzymes. Chondrocytes were pretreated with DMSO and IL-1β (20 ng/ml) for 24 h, and were then treated with AZ (25, 50 and 100 µM) for another 24 or 48 h. (A) Cell viability was assessed using the Cell Counting Kit-8 assay. (B) EdU staining (red fluorescence) was used to assess cell proliferation. (C) Expression levels of aggrecan and COL2A1. (D) ImageJ was used to analyze the relative protein expression levels of aggrecan, COL2A1, ADAMTS-4, iNOS, MMP13 and COX2. (E) ADAMTS-4, iNOS, MMP13 and COX2 were detected by western blotting. # P<0.05 vs. control; *P<0.05 vs. IL-1β. AZ, acetyl zingerone; COL2A1, collagen type II α1; COX2, cyclooxygenase 2; EdU, 5-ethynyl-2′-deoxyuridine; iNOS, inducible nitric oxide synthase.

Techniques: Expressing, Cell Counting, Staining, Fluorescence, Western Blot, Control

Journal: Molecular Medicine Reports

Article Title: Acetyl zingerone ameliorates osteoarthritis by inhibiting chondrocyte programmed cell death

doi: 10.3892/mmr.2023.13089

Figure Lengend Snippet: AZ inhibits IL-1β-induced ferroptosis in chondrocytes. (A) GSH and (B) MDA levels were measured in each group using GSH and MDA assays. Chondrocytes were pretreated with IL-1β (20 ng/ml) or Fer-1 (60 nmol/ml) for 24 h and then treated with or without AZ (100 µM) for an additional 24 h. (C) Mitochondria were observed by transmission electron microscopy. (D) GPX4 staining to indicate ferroptosis in mice following DMM surgery. (E) Cells were observed by fluorescence microscopy. (F) Chondrocytes were pretreated with or without IL-1β (20 ng/ml) or Fer-1 (60 nmol/ml) for 24 h and then treated with AZ (100 µM) for another 24 h, and GPX4 expression was determined by western blotting. # P<0.05 vs. control; *P<0.05 vs. IL-1β. AZ, acetyl zingerone; DMM, destabilization of the medial meniscus; Fer-1, ferrostatin-1; GPX4, glutathione peroxidase 4; GSH, glutathione; MDA, malondialdehyde.

Techniques: Transmission Assay, Electron Microscopy, Staining, Fluorescence, Microscopy, Expressing, Western Blot, Control

Journal: Molecular Medicine Reports

Article Title: Acetyl zingerone ameliorates osteoarthritis by inhibiting chondrocyte programmed cell death

doi: 10.3892/mmr.2023.13089

Figure Lengend Snippet: AZ inhibits ferroptosis in osteoarthritis through the Nrf2/HO-1 pathway. Chondrocytes were pretreated with IL-1β (20 ng/ml) for 24 h, with or without ML385 (Nrf2 inhibitors) or Fer-1 (60 nmol/ml) for 12 h, and then treated with or without AZ (100 µM) for an additional 24 h. (A) Protein expression levels of Nrf2, HO-1 and GPX4 was determined by western blotting. (B) Nrf2 staining of ferroptosis in chondrocytes. Chondrocytes were pretreated with IL-1β (20 ng/ml) for 24 h, with or without tin protoporphyrin IX (HO-1 inhibitors) or Fer-1 (60 nmol/ml) for 12 h, and then treated with or without AZ (100 µM) for an additional 24 h. (C) Protein expression levels of Nrf2, HO-1 and GPX4 was determined by western blotting. (D) Schematic diagram showing how AZ affects ferroptosis through the Nrf2/HO-1 signaling pathway. AZ, acetyl zingerone; DMM, destabilization of the medial meniscus; Fer-1, ferrostatin-1; GPX, glutathione peroxidase 4; HO-1, heme oxygenase-1; Nrf2, nuclear factor erythroid 2-related factor 2.

Techniques: Expressing, Western Blot, Staining

Morphological identification of bovine chondrocytes. (A) Toluidine blue staining of bovine chondrocytes. (B) Type II collagen α1 immunohistochemical staining.

Journal: Frontiers in Pharmacology

Article Title: Strontium Regulates the Proliferation and Differentiation of Isolated Primary Bovine Chondrocytes via the TGFβ/SMAD Pathway

doi: 10.3389/fphar.2022.925302

Figure Lengend Snippet: Morphological identification of bovine chondrocytes. (A) Toluidine blue staining of bovine chondrocytes. (B) Type II collagen α1 immunohistochemical staining.

Article Snippet: Membranes were blocked with 5% skimmed milk or BSA solution in TBS-T buffer for 2 h, and incubated overnight at 4°C with antibodies including type II Collagen α1 (COL2A1, 1:1000, AF6528, Beyotime Biotechnology, China), aggrecan (ACAN, 1:500, NB110-6524, Novusbio biologicals, United States), type X Collagen α1 (COL10A1, 1:500, bs0554R, Bioss biotechnology, China), Osteopontin (OPN, 1:1000, also called SPP1, secreted phosphoprotein 1, bs0019R, Bioss biotechnology, China), vascular endothelial growth factor (VEGFA, 1:1000, NB110-2381ss, Novus Bio biologicals, United States), alkaline phosphatase (ALPL, 1:1000, DF6225, Affinity, United States), SMAD3 (1:500, NB100-56479ss, Novusbio biologicals, United States), pSMAD3 (1:1000, 9520T, Cell Signaling Technology, United States), SMAD1/5/9 (1:1000, AF0614, Affinity, United States), pSMAD1/5/9 (1:1000, 13820T, Cell Signaling Technology, United States) and runt-related transcription factor 2 (RUNX2, 1:1000, AF5189, Affinity, United States).

Techniques: Staining, Immunohistochemical staining

Effects of Sr and SB-505124 on the transforming growth factor β (TGFβ)/SMAD family member (SMAD) signaling pathway and downstream gene transcription in bovine chondrocytes. Chondrocytes were treated with different doses of Sr (0, 0.1, 1, 10 μg/ml) with or without activin receptor-like kinase 5 (ALK5) kinase inhibitor (10 μM SB-505124). (A) Western blot analysis and relative protein expression levels of SMAD3, pSMAD3, SMAD1/5/9, pSMAD1/5/9, TGFβ, bone morphogenetic protein 2 (BMP2), and runt-related transcription factor 2 (RUNX2). (B) mRNA expression levels of TGFβ1, serpin family E member 1 (SERPINE1), ALK5, ALK1, and inhibitor of DNA binding 1 (ID1). All experiments were repeated at least thrice. Data are means ± SEM ( n = 3 in each group) * p < 0.05; ** p < 0.01.

Journal: Frontiers in Pharmacology

Article Title: Strontium Regulates the Proliferation and Differentiation of Isolated Primary Bovine Chondrocytes via the TGFβ/SMAD Pathway

doi: 10.3389/fphar.2022.925302

Figure Lengend Snippet: Effects of Sr and SB-505124 on the transforming growth factor β (TGFβ)/SMAD family member (SMAD) signaling pathway and downstream gene transcription in bovine chondrocytes. Chondrocytes were treated with different doses of Sr (0, 0.1, 1, 10 μg/ml) with or without activin receptor-like kinase 5 (ALK5) kinase inhibitor (10 μM SB-505124). (A) Western blot analysis and relative protein expression levels of SMAD3, pSMAD3, SMAD1/5/9, pSMAD1/5/9, TGFβ, bone morphogenetic protein 2 (BMP2), and runt-related transcription factor 2 (RUNX2). (B) mRNA expression levels of TGFβ1, serpin family E member 1 (SERPINE1), ALK5, ALK1, and inhibitor of DNA binding 1 (ID1). All experiments were repeated at least thrice. Data are means ± SEM ( n = 3 in each group) * p < 0.05; ** p < 0.01.

Techniques: Western Blot, Expressing, Binding Assay

Effects of Sr and SB-505124 on proliferation-related factors in bovine chondrocytes. Chondrocytes were treated with different doses of Sr (0, 0.1, 1, 10 μg/ml) with or without activin receptor-like kinase 5 (ALK5) kinase inhibitor (10 μM SB-505124). (A) Relative mRNA expression levels of type Ⅱ Collagen α1 (COL2A1) and aggrecan (ACAN). (B) Western blot and protein expression levels of COL2A1 and ACAN. All experiments were repeated at least thrice. Data are means ± SEM ( n = 3 in each group) * p < 0.05; ** p < 0.01.

Journal: Frontiers in Pharmacology

Article Title: Strontium Regulates the Proliferation and Differentiation of Isolated Primary Bovine Chondrocytes via the TGFβ/SMAD Pathway

doi: 10.3389/fphar.2022.925302

Figure Lengend Snippet: Effects of Sr and SB-505124 on proliferation-related factors in bovine chondrocytes. Chondrocytes were treated with different doses of Sr (0, 0.1, 1, 10 μg/ml) with or without activin receptor-like kinase 5 (ALK5) kinase inhibitor (10 μM SB-505124). (A) Relative mRNA expression levels of type Ⅱ Collagen α1 (COL2A1) and aggrecan (ACAN). (B) Western blot and protein expression levels of COL2A1 and ACAN. All experiments were repeated at least thrice. Data are means ± SEM ( n = 3 in each group) * p < 0.05; ** p < 0.01.

Techniques: Expressing, Western Blot

Cell cycle changes in bovine chondrocytes treated with different doses of Sr (0, 0.1, 1, 10 μg/mL). (A) Representative histograms of flow cytometry analysis of the cell cycle in bovine chondrocytes. (B) Representative images of cell cycle distribution. (C) Proliferation index (PI) was calculated based on the equation: PI = (S + G2/M)/(S + G2/M + G0/G1). Data are means ± SEM ( n = 3 in each group) * p < 0.05; ** p < 0.01.

Journal: Frontiers in Pharmacology

Article Title: Strontium Regulates the Proliferation and Differentiation of Isolated Primary Bovine Chondrocytes via the TGFβ/SMAD Pathway

doi: 10.3389/fphar.2022.925302

Figure Lengend Snippet: Cell cycle changes in bovine chondrocytes treated with different doses of Sr (0, 0.1, 1, 10 μg/mL). (A) Representative histograms of flow cytometry analysis of the cell cycle in bovine chondrocytes. (B) Representative images of cell cycle distribution. (C) Proliferation index (PI) was calculated based on the equation: PI = (S + G2/M)/(S + G2/M + G0/G1). Data are means ± SEM ( n = 3 in each group) * p < 0.05; ** p < 0.01.

Techniques: Flow Cytometry

The effect of Sr on the cytoskeleton in bovine chondrocytes stained with Coomassie blue. (A) 0 μg/ml. (B) 0.1 μg/ml. (C) 1 μg/ml. (D) 10 μg/ml.

Journal: Frontiers in Pharmacology

Article Title: Strontium Regulates the Proliferation and Differentiation of Isolated Primary Bovine Chondrocytes via the TGFβ/SMAD Pathway

doi: 10.3389/fphar.2022.925302

Figure Lengend Snippet: The effect of Sr on the cytoskeleton in bovine chondrocytes stained with Coomassie blue. (A) 0 μg/ml. (B) 0.1 μg/ml. (C) 1 μg/ml. (D) 10 μg/ml.

Techniques: Staining

Effects of Sr and SB-505124 on differentiation-related factors in bovine chondrocytes. Chondrocytes were treated with different doses of Sr (0, 0.1, 1, 10 μg/ml) with or without activin receptor-like kinase 5 (ALK5) kinase inhibitor (10 μM SB-505124). (A) Western blot and protein expression levels of secreted phosphoprotein 1 (SPP1), alkaline phosphatase (ALPL), vascular endothelial growth factor (VEGFA), and type Ⅹ Collagen α1 (COL10A1). (B) mRNA expression levels of SPP1, ALPL, VEGFA, and COL10A1. All experiments were repeated at least thrice. Data are means ± SEM ( n = 3 in each group) * p < 0.05; ** p < 0.01.

Journal: Frontiers in Pharmacology

Article Title: Strontium Regulates the Proliferation and Differentiation of Isolated Primary Bovine Chondrocytes via the TGFβ/SMAD Pathway

doi: 10.3389/fphar.2022.925302

Figure Lengend Snippet: Effects of Sr and SB-505124 on differentiation-related factors in bovine chondrocytes. Chondrocytes were treated with different doses of Sr (0, 0.1, 1, 10 μg/ml) with or without activin receptor-like kinase 5 (ALK5) kinase inhibitor (10 μM SB-505124). (A) Western blot and protein expression levels of secreted phosphoprotein 1 (SPP1), alkaline phosphatase (ALPL), vascular endothelial growth factor (VEGFA), and type Ⅹ Collagen α1 (COL10A1). (B) mRNA expression levels of SPP1, ALPL, VEGFA, and COL10A1. All experiments were repeated at least thrice. Data are means ± SEM ( n = 3 in each group) * p < 0.05; ** p < 0.01.

Techniques: Western Blot, Expressing

Schematic of the proposed mechanism whereby Sr affects proliferation and differentiation of bovine chondrocytes via the transforming growth factor β (TGFβ) signaling pathway. Sr shifts the signaling of TGFβ1 to SMAD family member 3 (SMAD3) by promoting activin receptor-like kinase 5 (ALK5) expression and inhibiting ALK1 expression. Phosphorylation of SMAD3 and SMAD1/5/9 after binding with SMAD4 transfers them into the nucleus to regulate gene transcription. An increase in pSMAD3 promotes the expression of type Ⅱ Collagen α1 (COL2A1) and aggrecan (ACAN). pSMAD1/5/9 induces type Ⅹ Collagen α1 (COL10A1), secreted phosphoprotein 1 (SPP1), vascular endothelial growth factor (VEGFA), and alkaline phosphatase (ALPL) by stimulating the function of runt-related transcription factor 2 (RUNX2). The increase in the pSMAD3 can inhibit the function of RUNX2 to decrease the COL10A1, SPP1, and ALPL expression.

Journal: Frontiers in Pharmacology

Article Title: Strontium Regulates the Proliferation and Differentiation of Isolated Primary Bovine Chondrocytes via the TGFβ/SMAD Pathway

doi: 10.3389/fphar.2022.925302

Figure Lengend Snippet: Schematic of the proposed mechanism whereby Sr affects proliferation and differentiation of bovine chondrocytes via the transforming growth factor β (TGFβ) signaling pathway. Sr shifts the signaling of TGFβ1 to SMAD family member 3 (SMAD3) by promoting activin receptor-like kinase 5 (ALK5) expression and inhibiting ALK1 expression. Phosphorylation of SMAD3 and SMAD1/5/9 after binding with SMAD4 transfers them into the nucleus to regulate gene transcription. An increase in pSMAD3 promotes the expression of type Ⅱ Collagen α1 (COL2A1) and aggrecan (ACAN). pSMAD1/5/9 induces type Ⅹ Collagen α1 (COL10A1), secreted phosphoprotein 1 (SPP1), vascular endothelial growth factor (VEGFA), and alkaline phosphatase (ALPL) by stimulating the function of runt-related transcription factor 2 (RUNX2). The increase in the pSMAD3 can inhibit the function of RUNX2 to decrease the COL10A1, SPP1, and ALPL expression.

Techniques: Expressing, Phospho-proteomics, Binding Assay

Figure 1. The cytotoxicity of AnTT (A) and PT3 (B) on SW1353 chondrocytes upon 24 h treatment. The results were obtained from 3 independent experiments with 4 technical replicates during mea- surement. The data were displayed in mean ± SEM. *** indicates a signiﬁcant difference (p < 0.001) compared to the VC (0 µg/mL).

Journal: Applied Sciences

Article Title: Protective Effects of Annatto Tocotrienol and Palm Tocotrienol-Rich Fraction on Chondrocytes Exposed to Monosodium Iodoacetate

doi: 10.3390/app11209643

Figure Lengend Snippet: Figure 1. The cytotoxicity of AnTT (A) and PT3 (B) on SW1353 chondrocytes upon 24 h treatment. The results were obtained from 3 independent experiments with 4 technical replicates during mea- surement. The data were displayed in mean ± SEM. *** indicates a signiﬁcant difference (p < 0.001) compared to the VC (0 µg/mL).

Article Snippet: The human collagen type I α1 (COL1α1; catalogue no. E-EL-H0869), collagen type II α1 (COL2α1; catalogue no. E-EL-H0777), sex-determining region Y box protein 9 (SOX9; catalogue no. E-EL-H1349), a disintegrin and metalloproteinase with thrombospondin type 1 Motif 4 (ADAMTS4; catalogue no. E-EL-H0266) and aggrecan (catalogue no. E-EL-H0294) levels were determined by using the sandwiched ELISA kits from Elabscience (Houston, Texas, USA) according to the manufacturer’s protocol.

Techniques:

$Figure 6. Proposed mechanism of action of tocotrienols on chondrocytes. Both AnTT and PT3 suppress oxidative stress induced by MIA. AnTT also enhances the self-repair mechanism and anabolic activities of chondrocytes exposed to MIA. Abbreviations: ↑, cause or induce; ⊺, inhibit; AnTT, annatto tocotrienols; COL2α1, collagen type II α1; PT3, palm tocotrienol-rich fraction; SOX9, sex-determining region Y box protein 9.$

Journal: Applied Sciences

Article Title: Protective Effects of Annatto Tocotrienol and Palm Tocotrienol-Rich Fraction on Chondrocytes Exposed to Monosodium Iodoacetate

doi: 10.3390/app11209643

Figure Lengend Snippet: Figure 6. Proposed mechanism of action of tocotrienols on chondrocytes. Both AnTT and PT3 suppress oxidative stress induced by MIA. AnTT also enhances the self-repair mechanism and anabolic activities of chondrocytes exposed to MIA. Abbreviations: ↑, cause or induce; ⊺, inhibit; AnTT, annatto tocotrienols; COL2α1, collagen type II α1; PT3, palm tocotrienol-rich fraction; SOX9, sex-determining region Y box protein 9.

Techniques:

Review

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1) Product Images from "Acetyl zingerone ameliorates osteoarthritis by inhibiting chondrocyte programmed cell death"

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