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TGF-β1 actives <t>AKT,</t> Smad3 and MAPK pathways in DPSCs. (A) Western blot analysis of <t>p-AKT,</t> AKT, p-p38 MAPK, p38 MAPK, p-Smad3, Smad3, p-JNK, JNK, p-Erk and Erk from DPSCs treated with 1 ng/mL TGF-β1 in a time course. (B) Western blot analysis of p-AKT, p-p38, p-Smad3, p-JNK, p-Erk in DPSCs after treatment with pathways inhibitor respectively for 1 h. Error bars = means ± standard deviation (SD), n = 3, ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001. AKT, protein kinase B; DPSCs, dental pulp stem cells; Erk 1/2, extracellular signal-regulated kinase 1/2; JNK, c-Jun N-terminal kinase and; p38 MAPK, p38 mitogen-activated protein kinase; Smad3, small mothers against decapentaplegic 3; TGF-β1, Transforming growth factor-β1.
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TGF-β1 actives <t>AKT,</t> Smad3 and MAPK pathways in DPSCs. (A) Western blot analysis of <t>p-AKT,</t> AKT, p-p38 MAPK, p38 MAPK, p-Smad3, Smad3, p-JNK, JNK, p-Erk and Erk from DPSCs treated with 1 ng/mL TGF-β1 in a time course. (B) Western blot analysis of p-AKT, p-p38, p-Smad3, p-JNK, p-Erk in DPSCs after treatment with pathways inhibitor respectively for 1 h. Error bars = means ± standard deviation (SD), n = 3, ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001. AKT, protein kinase B; DPSCs, dental pulp stem cells; Erk 1/2, extracellular signal-regulated kinase 1/2; JNK, c-Jun N-terminal kinase and; p38 MAPK, p38 mitogen-activated protein kinase; Smad3, small mothers against decapentaplegic 3; TGF-β1, Transforming growth factor-β1.
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TGF-β1 actives AKT, Smad3 and MAPK pathways in DPSCs. (A) Western blot analysis of p-AKT, AKT, p-p38 MAPK, p38 MAPK, p-Smad3, Smad3, p-JNK, JNK, p-Erk and Erk from DPSCs treated with 1 ng/mL TGF-β1 in a time course. (B) Western blot analysis of p-AKT, p-p38, p-Smad3, p-JNK, p-Erk in DPSCs after treatment with pathways inhibitor respectively for 1 h. Error bars = means ± standard deviation (SD), n = 3, ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001. AKT, protein kinase B; DPSCs, dental pulp stem cells; Erk 1/2, extracellular signal-regulated kinase 1/2; JNK, c-Jun N-terminal kinase and; p38 MAPK, p38 mitogen-activated protein kinase; Smad3, small mothers against decapentaplegic 3; TGF-β1, Transforming growth factor-β1.

Journal: Journal of Dental Sciences

Article Title: Transforming growth factor-β1 promotes early odontoblastic differentiation of dental pulp stem cells via activating AKT, Erk1/2 and p38 MAPK pathways

doi: 10.1016/j.jds.2022.06.027

Figure Lengend Snippet: TGF-β1 actives AKT, Smad3 and MAPK pathways in DPSCs. (A) Western blot analysis of p-AKT, AKT, p-p38 MAPK, p38 MAPK, p-Smad3, Smad3, p-JNK, JNK, p-Erk and Erk from DPSCs treated with 1 ng/mL TGF-β1 in a time course. (B) Western blot analysis of p-AKT, p-p38, p-Smad3, p-JNK, p-Erk in DPSCs after treatment with pathways inhibitor respectively for 1 h. Error bars = means ± standard deviation (SD), n = 3, ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001. AKT, protein kinase B; DPSCs, dental pulp stem cells; Erk 1/2, extracellular signal-regulated kinase 1/2; JNK, c-Jun N-terminal kinase and; p38 MAPK, p38 mitogen-activated protein kinase; Smad3, small mothers against decapentaplegic 3; TGF-β1, Transforming growth factor-β1.

Article Snippet: After blocking in QuickBlock Blocking Buffer (Beyotime) for 20 min, the membrane was incubated overnight at 4 °C with primary antibodies as follows: anti-AKT, anti-phosphor-AKT (p-AKT), anti-Erk1/2, anti-p-Erk1/2, anti-p38 MAPK, anti-p-p38 MAPK, anti-Smad3, anti-p-Smad3, anti-JNK, anti-p-JNK, anti-collagen type 1 alpha 1 (COL1A), anti-runt-related transcription factor 2 (Runx2) (1:1000; all purchased from CST, Boston, MA, USA), anti-dentin matrix protein-1 (DMP-1) (1:1000; Novus, Littleton, CO, USA) and anti-glyceraldenhyde-3-phosphate dehydrogenase (GAPDH) (1:10000; Proteintech, Rosemont, IL, USA).

Techniques: Western Blot, Standard Deviation

Involvement of p38 MAPK, Erk1/2 and AKT signaling in the TGF-β1-induced early odontoblastic differentiation of DPSCs. ( A) ALP activities and ALP staining in the control group, TGF-β1 treated groups with or without pathways inhibitors at day 7(50×). (B) The protein expressions of DMP-1, COL1A, and Runx2 in different groups at day 7. Scale bars are shown. Error bars = means ± standard deviation (SD), n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001. NS P > 0.5. COL1A, collagen type 1 alpha 1; DPSCs, dental pulp stem cells; DMP-1, dentin matrix protein 1; Runx2, runt-related transcription factor 2; TGF-β1, Transforming growth factor-β1.

Journal: Journal of Dental Sciences

Article Title: Transforming growth factor-β1 promotes early odontoblastic differentiation of dental pulp stem cells via activating AKT, Erk1/2 and p38 MAPK pathways

doi: 10.1016/j.jds.2022.06.027

Figure Lengend Snippet: Involvement of p38 MAPK, Erk1/2 and AKT signaling in the TGF-β1-induced early odontoblastic differentiation of DPSCs. ( A) ALP activities and ALP staining in the control group, TGF-β1 treated groups with or without pathways inhibitors at day 7(50×). (B) The protein expressions of DMP-1, COL1A, and Runx2 in different groups at day 7. Scale bars are shown. Error bars = means ± standard deviation (SD), n = 3. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001. NS P > 0.5. COL1A, collagen type 1 alpha 1; DPSCs, dental pulp stem cells; DMP-1, dentin matrix protein 1; Runx2, runt-related transcription factor 2; TGF-β1, Transforming growth factor-β1.

Article Snippet: After blocking in QuickBlock Blocking Buffer (Beyotime) for 20 min, the membrane was incubated overnight at 4 °C with primary antibodies as follows: anti-AKT, anti-phosphor-AKT (p-AKT), anti-Erk1/2, anti-p-Erk1/2, anti-p38 MAPK, anti-p-p38 MAPK, anti-Smad3, anti-p-Smad3, anti-JNK, anti-p-JNK, anti-collagen type 1 alpha 1 (COL1A), anti-runt-related transcription factor 2 (Runx2) (1:1000; all purchased from CST, Boston, MA, USA), anti-dentin matrix protein-1 (DMP-1) (1:1000; Novus, Littleton, CO, USA) and anti-glyceraldenhyde-3-phosphate dehydrogenase (GAPDH) (1:10000; Proteintech, Rosemont, IL, USA).

Techniques: Staining, Control, Standard Deviation

Schematic illustration showing the molecular mechanism of TGF-β1 on early odontoblastic differentiation of DPSCs. AKT, protein kinase B; DPSCs, dental pulp stem cells; Erk 1/2, extracellular signal-regulated kinase 1/2; JNK, c-Jun N-terminal kinase and; p38 MAPK, p38 mitogen-activated protein kinase; Smad3, small mothers against decapentaplegic 3; TGF-β1, Transforming growth factor-β1.

Journal: Journal of Dental Sciences

Article Title: Transforming growth factor-β1 promotes early odontoblastic differentiation of dental pulp stem cells via activating AKT, Erk1/2 and p38 MAPK pathways

doi: 10.1016/j.jds.2022.06.027

Figure Lengend Snippet: Schematic illustration showing the molecular mechanism of TGF-β1 on early odontoblastic differentiation of DPSCs. AKT, protein kinase B; DPSCs, dental pulp stem cells; Erk 1/2, extracellular signal-regulated kinase 1/2; JNK, c-Jun N-terminal kinase and; p38 MAPK, p38 mitogen-activated protein kinase; Smad3, small mothers against decapentaplegic 3; TGF-β1, Transforming growth factor-β1.

Article Snippet: After blocking in QuickBlock Blocking Buffer (Beyotime) for 20 min, the membrane was incubated overnight at 4 °C with primary antibodies as follows: anti-AKT, anti-phosphor-AKT (p-AKT), anti-Erk1/2, anti-p-Erk1/2, anti-p38 MAPK, anti-p-p38 MAPK, anti-Smad3, anti-p-Smad3, anti-JNK, anti-p-JNK, anti-collagen type 1 alpha 1 (COL1A), anti-runt-related transcription factor 2 (Runx2) (1:1000; all purchased from CST, Boston, MA, USA), anti-dentin matrix protein-1 (DMP-1) (1:1000; Novus, Littleton, CO, USA) and anti-glyceraldenhyde-3-phosphate dehydrogenase (GAPDH) (1:10000; Proteintech, Rosemont, IL, USA).

Techniques: