The Experts below are selected from a list of 16245 Experts worldwide ranked by ideXlab platform
Werner Falk - One of the best experts on this subject based on the ideXlab platform.
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interferon gamma ifn γ and tumour necrosis factor tnf induced nitric oxide as toxic Effector Molecule in chronic dextran sulphate sodium dss induced colitis in mice
Clinical and Experimental Immunology, 1999Co-Authors: F Obermeier, G Kojouharoff, W Hans, J Scholmerich, V Gross, Werner FalkAbstract:Excess nitric oxide formation caused by the activity of the inducible nitric oxide synthase has been implicated as a toxic Effector Molecule in the pathogenesis of experimental colitis and inflammatory bowel disease. It was therefore investigated whether inhibition of this synthase or the cytokines TNF and IFN-γ, inducers of nitric oxide synthase, had effects on chronic colitis in mice. Chronic colitis was induced in mice by repeated feeding of DSS. Cytokines were neutralized by treatment with MoAbs and nitric oxide synthase was inhibited by aminoguanidine. The degree of colonic inflammation was assessed by a histological score and colon length. Aminoguanidine treatment reduced nitric oxide activity by 60% (P = 0.0004), the histological score by 31% (P = 0.005) and increased colon length by 1.4 cm (P = 0.002). Neutralization of TNF and IFN-γ resulted in increased colon length (0.7 cm, P = 0.07 and 0.8 cm, P = 0.03), improved histological score (19%, P = 0.045 and 25%, P = 0.013), and reduced nitric oxide activity (31%, P = 0.07 and 54%, P = 0.004) compared with controls. The combination of anti-cytokine treatments had additive effects. TNF and IFN-γ are involved in perpetuation of chronic DSS-induced colitis, and induction of excessive nitric oxide activity could be their common Effector mechanism.
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interferon gamma ifn gamma and tumour necrosis factor tnf induced nitric oxide as toxic Effector Molecule in chronic dextran sulphate sodium dss induced colitis in mice
Clinical and Experimental Immunology, 1999Co-Authors: F Obermeier, G Kojouharoff, W Hans, J Scholmerich, V Gross, Werner FalkAbstract:Excess nitric oxide formation caused by the activity of the inducible nitric oxide synthase has been implicated as a toxic Effector Molecule in the pathogenesis of experimental colitis and inflammatory bowel disease. It was therefore investigated whether inhibition of this synthase or the cytokines TNF and IFN-gamma, inducers of nitric oxide synthase, had effects on chronic colitis in mice. Chronic colitis was induced in mice by repeated feeding of DSS. Cytokines were neutralized by treatment with MoAbs and nitric oxide synthase was inhibited by aminoguanidine. The degree of colonic inflammation was assessed by a histological score and colon length. Aminoguanidine treatment reduced nitric oxide activity by 60% (P = 0. 0004), the histological score by 31% (P = 0.005) and increased colon length by 1.4 cm (P = 0.002). Neutralization of TNF and IFN-gamma resulted in increased colon length (0.7 cm, P = 0.07 and 0.8 cm, P = 0.03), improved histological score (19%, P = 0.045 and 25%, P = 0. 013), and reduced nitric oxide activity (31%, P = 0.07 and 54%, P = 0.004) compared with controls. The combination of anti-cytokine treatments had additive effects. TNF and IFN-gamma are involved in perpetuation of chronic DSS-induced colitis, and induction of excessive nitric oxide activity could be their common Effector mechanism.
Joji Kusuyama - One of the best experts on this subject based on the ideXlab platform.
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bone morphogenetic protein 9 bmp9 directly induces notch Effector Molecule hes1 through the smad signaling pathway in osteoblasts
FEBS Letters, 2021Co-Authors: Changhwan Seong, Norika Chiba, Joji Kusuyama, Muhammad Subhan Amir, Nahoko Eiraku, Sachiko Yamashita, Tomokazu OhnishiAbstract:Bone morphogenetic protein (BMP) 9 is one of the most osteogenic BMPs, but its mechanism of action has not been fully elucidated. Hes1, a transcriptional regulator with a basic helix-loop-helix domain, is a well-known Effector of Notch signaling. Here, we find that BMP9 induces periodic increases of Hes1 mRNA and protein expression in osteoblasts, presumably through an autocrine negative feedback mechanism. BMP9-mediated Hes1 induction is significantly inhibited by an ALK inhibitor and overexpression of Smad7, an inhibitory Smad. Luciferase and ChIP assays revealed that two Smad-binding sites in the 5' upstream region of the mouse Hes1 gene are essential for transcriptional activation by BMP9. Thus, our data indicate that BMP9 induces Hes1 expression in osteoblasts via the Smad signaling pathway.
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bone morphogenetic protein 9 bmp9 directly induces notch Effector Molecule hes1 through the smad signaling pathway in osteoblasts
FEBS Letters, 2020Co-Authors: Changhwan Seong, Norika Chiba, Joji Kusuyama, Muhammad Subhan Amir, Nahoko Eiraku, Sachiko Yamashita, Tomokazu OhnishiAbstract:Bone morphogenetic protein (BMP) 9 is one of the most osteogenic BMPs, but its mechanism of action has not been fully elucidated. Hes1, a transcriptional regulator with a basic helix-loop-helix (bHLH) domain, is a well-known Effector of Notch signaling. Here, we find that BMP9 induces periodic increases of Hes1 mRNA and protein expression in osteoblasts, presumably through an autocrine negative feedback mechanism. BMP9-mediated Hes1 induction is significantly inhibited by an ALK inhibitor and overexpression of Smad7, an inhibitory Smad. Luciferase and chromatin immunoprecipitation assays revealed that two Smad binding sites in the 5' upstream region of the mouse Hes1 gene are essential for transcriptional activation by BMP9. Thus, our data indicate that BMP9 induces Hes1 expression in osteoblasts via the Smad signaling pathway.
F Obermeier - One of the best experts on this subject based on the ideXlab platform.
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interferon gamma ifn γ and tumour necrosis factor tnf induced nitric oxide as toxic Effector Molecule in chronic dextran sulphate sodium dss induced colitis in mice
Clinical and Experimental Immunology, 1999Co-Authors: F Obermeier, G Kojouharoff, W Hans, J Scholmerich, V Gross, Werner FalkAbstract:Excess nitric oxide formation caused by the activity of the inducible nitric oxide synthase has been implicated as a toxic Effector Molecule in the pathogenesis of experimental colitis and inflammatory bowel disease. It was therefore investigated whether inhibition of this synthase or the cytokines TNF and IFN-γ, inducers of nitric oxide synthase, had effects on chronic colitis in mice. Chronic colitis was induced in mice by repeated feeding of DSS. Cytokines were neutralized by treatment with MoAbs and nitric oxide synthase was inhibited by aminoguanidine. The degree of colonic inflammation was assessed by a histological score and colon length. Aminoguanidine treatment reduced nitric oxide activity by 60% (P = 0.0004), the histological score by 31% (P = 0.005) and increased colon length by 1.4 cm (P = 0.002). Neutralization of TNF and IFN-γ resulted in increased colon length (0.7 cm, P = 0.07 and 0.8 cm, P = 0.03), improved histological score (19%, P = 0.045 and 25%, P = 0.013), and reduced nitric oxide activity (31%, P = 0.07 and 54%, P = 0.004) compared with controls. The combination of anti-cytokine treatments had additive effects. TNF and IFN-γ are involved in perpetuation of chronic DSS-induced colitis, and induction of excessive nitric oxide activity could be their common Effector mechanism.
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interferon gamma ifn gamma and tumour necrosis factor tnf induced nitric oxide as toxic Effector Molecule in chronic dextran sulphate sodium dss induced colitis in mice
Clinical and Experimental Immunology, 1999Co-Authors: F Obermeier, G Kojouharoff, W Hans, J Scholmerich, V Gross, Werner FalkAbstract:Excess nitric oxide formation caused by the activity of the inducible nitric oxide synthase has been implicated as a toxic Effector Molecule in the pathogenesis of experimental colitis and inflammatory bowel disease. It was therefore investigated whether inhibition of this synthase or the cytokines TNF and IFN-gamma, inducers of nitric oxide synthase, had effects on chronic colitis in mice. Chronic colitis was induced in mice by repeated feeding of DSS. Cytokines were neutralized by treatment with MoAbs and nitric oxide synthase was inhibited by aminoguanidine. The degree of colonic inflammation was assessed by a histological score and colon length. Aminoguanidine treatment reduced nitric oxide activity by 60% (P = 0. 0004), the histological score by 31% (P = 0.005) and increased colon length by 1.4 cm (P = 0.002). Neutralization of TNF and IFN-gamma resulted in increased colon length (0.7 cm, P = 0.07 and 0.8 cm, P = 0.03), improved histological score (19%, P = 0.045 and 25%, P = 0. 013), and reduced nitric oxide activity (31%, P = 0.07 and 54%, P = 0.004) compared with controls. The combination of anti-cytokine treatments had additive effects. TNF and IFN-gamma are involved in perpetuation of chronic DSS-induced colitis, and induction of excessive nitric oxide activity could be their common Effector mechanism.
Tomokazu Ohnishi - One of the best experts on this subject based on the ideXlab platform.
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bone morphogenetic protein 9 bmp9 directly induces notch Effector Molecule hes1 through the smad signaling pathway in osteoblasts
FEBS Letters, 2021Co-Authors: Changhwan Seong, Norika Chiba, Joji Kusuyama, Muhammad Subhan Amir, Nahoko Eiraku, Sachiko Yamashita, Tomokazu OhnishiAbstract:Bone morphogenetic protein (BMP) 9 is one of the most osteogenic BMPs, but its mechanism of action has not been fully elucidated. Hes1, a transcriptional regulator with a basic helix-loop-helix domain, is a well-known Effector of Notch signaling. Here, we find that BMP9 induces periodic increases of Hes1 mRNA and protein expression in osteoblasts, presumably through an autocrine negative feedback mechanism. BMP9-mediated Hes1 induction is significantly inhibited by an ALK inhibitor and overexpression of Smad7, an inhibitory Smad. Luciferase and ChIP assays revealed that two Smad-binding sites in the 5' upstream region of the mouse Hes1 gene are essential for transcriptional activation by BMP9. Thus, our data indicate that BMP9 induces Hes1 expression in osteoblasts via the Smad signaling pathway.
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bone morphogenetic protein 9 bmp9 directly induces notch Effector Molecule hes1 through the smad signaling pathway in osteoblasts
FEBS Letters, 2020Co-Authors: Changhwan Seong, Norika Chiba, Joji Kusuyama, Muhammad Subhan Amir, Nahoko Eiraku, Sachiko Yamashita, Tomokazu OhnishiAbstract:Bone morphogenetic protein (BMP) 9 is one of the most osteogenic BMPs, but its mechanism of action has not been fully elucidated. Hes1, a transcriptional regulator with a basic helix-loop-helix (bHLH) domain, is a well-known Effector of Notch signaling. Here, we find that BMP9 induces periodic increases of Hes1 mRNA and protein expression in osteoblasts, presumably through an autocrine negative feedback mechanism. BMP9-mediated Hes1 induction is significantly inhibited by an ALK inhibitor and overexpression of Smad7, an inhibitory Smad. Luciferase and chromatin immunoprecipitation assays revealed that two Smad binding sites in the 5' upstream region of the mouse Hes1 gene are essential for transcriptional activation by BMP9. Thus, our data indicate that BMP9 induces Hes1 expression in osteoblasts via the Smad signaling pathway.
Muhammad Subhan Amir - One of the best experts on this subject based on the ideXlab platform.
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bone morphogenetic protein 9 bmp9 directly induces notch Effector Molecule hes1 through the smad signaling pathway in osteoblasts
FEBS Letters, 2021Co-Authors: Changhwan Seong, Norika Chiba, Joji Kusuyama, Muhammad Subhan Amir, Nahoko Eiraku, Sachiko Yamashita, Tomokazu OhnishiAbstract:Bone morphogenetic protein (BMP) 9 is one of the most osteogenic BMPs, but its mechanism of action has not been fully elucidated. Hes1, a transcriptional regulator with a basic helix-loop-helix domain, is a well-known Effector of Notch signaling. Here, we find that BMP9 induces periodic increases of Hes1 mRNA and protein expression in osteoblasts, presumably through an autocrine negative feedback mechanism. BMP9-mediated Hes1 induction is significantly inhibited by an ALK inhibitor and overexpression of Smad7, an inhibitory Smad. Luciferase and ChIP assays revealed that two Smad-binding sites in the 5' upstream region of the mouse Hes1 gene are essential for transcriptional activation by BMP9. Thus, our data indicate that BMP9 induces Hes1 expression in osteoblasts via the Smad signaling pathway.
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bone morphogenetic protein 9 bmp9 directly induces notch Effector Molecule hes1 through the smad signaling pathway in osteoblasts
FEBS Letters, 2020Co-Authors: Changhwan Seong, Norika Chiba, Joji Kusuyama, Muhammad Subhan Amir, Nahoko Eiraku, Sachiko Yamashita, Tomokazu OhnishiAbstract:Bone morphogenetic protein (BMP) 9 is one of the most osteogenic BMPs, but its mechanism of action has not been fully elucidated. Hes1, a transcriptional regulator with a basic helix-loop-helix (bHLH) domain, is a well-known Effector of Notch signaling. Here, we find that BMP9 induces periodic increases of Hes1 mRNA and protein expression in osteoblasts, presumably through an autocrine negative feedback mechanism. BMP9-mediated Hes1 induction is significantly inhibited by an ALK inhibitor and overexpression of Smad7, an inhibitory Smad. Luciferase and chromatin immunoprecipitation assays revealed that two Smad binding sites in the 5' upstream region of the mouse Hes1 gene are essential for transcriptional activation by BMP9. Thus, our data indicate that BMP9 induces Hes1 expression in osteoblasts via the Smad signaling pathway.
