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  1. Article ; Online: Smad signaling in skeletal development and regeneration.

    Song, Buer / Estrada, Kristine D / Lyons, Karen M

    Cytokine & growth factor reviews

    2009  Volume 20, Issue 5-6, Page(s) 379–388

    Abstract: ... of skeletal development and regeneration. ... target gene transcription. Both groups of growth factors play important roles in skeletal development and ... regeneration. However, whether these effects reflect signaling through canonical Smad pathways, or other non ...

    Abstract Smad proteins are intracellular molecules that mediate the canonical signaling cascade of TGFbeta superfamily growth factors. The TGFbeta superfamily comprises two groups of growth factors, BMPs and TGFbetas. Both groups can be further divided into several sub-groups based on sequence homologies and functional similarities. Ligands of the TGFbeta superfamily bind to cell surface receptors to activate Smad proteins in the cytoplasm; then the activated Smad proteins translocate into the nucleus to activate or repress specific target gene transcription. Both groups of growth factors play important roles in skeletal development and regeneration. However, whether these effects reflect signaling through canonical Smad pathways, or other non-canonical signaling pathways in vivo remains a mystery. Moreover, the mechanisms utilized by Smad proteins to initiate nuclear events and their interactions with cytoplasmic proteins are still under intensive investigation. This review will discuss the most recent progress understanding Smad signaling in the context of skeletal development and regeneration.
    MeSH term(s) Animals ; Bone Development/genetics ; Bone Development/physiology ; Bone Regeneration/genetics ; Bone Regeneration/physiology ; Chondrogenesis/genetics ; Chondrogenesis/physiology ; Humans ; Models, Biological ; Osteogenesis/genetics ; Osteogenesis/physiology ; Signal Transduction/genetics ; Signal Transduction/physiology ; Smad Proteins/genetics ; Smad Proteins/physiology ; TGF-beta Superfamily Proteins/genetics ; TGF-beta Superfamily Proteins/physiology
    Chemical Substances Smad Proteins ; TGF-beta Superfamily Proteins
    Language English
    Publishing date 2009-11-18
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1330534-7
    ISSN 1879-0305 ; 1359-6101
    ISSN (online) 1879-0305
    ISSN 1359-6101
    DOI 10.1016/j.cytogfr.2009.10.010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2653: Show issues Location:
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  2. Article ; Online: miR-122-5p negatively regulates the transforming growth factor-β/Smad signaling pathway in skeletal muscle myogenesis.

    Ding, Zheci / Lin, Jinrong / Sun, Yaying / Cong, Shuang / Liu, Shaohua / Zhang, Yuhan / Chen, Qingyan / Chen, Jiwu

    Cell biochemistry and function

    2019  Volume 38, Issue 2, Page(s) 231–238

    Abstract: ... we aimed to investigate the impact of miR-122 on skeletal muscle myogenesis and explore its underlying ... in skeletal muscle diseases and future translational studies on potential novel gene therapy for skeletal ... Regeneration remains a major challenge in skeletal muscle repair after injury. Recently ...

    Abstract Regeneration remains a major challenge in skeletal muscle repair after injury. Recently, transforming growth factor-β (TGF-β)/Smad pathway was found to play an important role in inhibiting myogenesis, a crucial stage in skeletal muscle regeneration. In our previous study, microRNA-122-5p (miR-122) was proved to have the function of downregulating TGF-β/Smad pathway. Theoretically, miR-122 might also be involved in the process of skeletal muscle myogenesis through the regulation of TGF-β/Smad pathway. In this study, we aimed to investigate the impact of miR-122 on skeletal muscle myogenesis and explore its underlying mechanism. Results showed that miR-122 and myogenic markers were downregulated in C2C12 cells after TGF-β stimulation, and miR-122 overexpression could restore the myogenesis inhibited by TGF-β. We then located TGFBR2 as the direct target of miR-122 and discovered the effect of miR-122 overexpression could be rescued by TGFBR2 overexpression. Further, the downstream molecules of TGFBR2 in the TGF-β/Smad pathway were found to be suppressed by miR-122. In conclusion, miR-122 could suppress the TGF-β/Smad signalling pathway by directly targeting TGFBR2 and, consequently, restore myogenesis. SIGNIFICANCE OF THE STUDY: Regeneration remains a major challenge in skeletal muscle repair after injury. In this study, it was found that miR-122 could suppress the TGF-β/Smad signalling pathway by directly targeting TGFBR2 and, consequently, restore myogenesis. Our findings could inspire future experiments on the role of miRs in skeletal muscle diseases and future translational studies on potential novel gene therapy for skeletal muscle injury.
    MeSH term(s) Animals ; Cell Line ; Cell Proliferation/drug effects ; HEK293 Cells ; Humans ; Mice ; MicroRNAs/metabolism ; Muscle Development ; Muscle, Skeletal/metabolism ; Receptor, Transforming Growth Factor-beta Type II/metabolism ; Regeneration ; Signal Transduction ; Smad Proteins/metabolism ; Transforming Growth Factor beta1/metabolism
    Chemical Substances MIRN122 microRNA, human ; MicroRNAs ; Mirn122 microRNA, mouse ; Smad Proteins ; TGFB1 protein, human ; Tgfb1 protein, mouse ; Transforming Growth Factor beta1 ; Receptor, Transforming Growth Factor-beta Type II (EC 2.7.11.30) ; TGFBR2 protein, human (EC 2.7.11.30) ; Tgfbr2 protein, mouse (EC 2.7.11.30)
    Language English
    Publishing date 2019-11-11
    Publishing country England
    Document type Journal Article
    ZDB-ID 283643-9
    ISSN 1099-0844 ; 0263-6484
    ISSN (online) 1099-0844
    ISSN 0263-6484
    DOI 10.1002/cbf.3460
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1994: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article: Mollugin enhances the osteogenic action of BMP-2 via the p38-Smad signaling pathway.

    Moon, Seong-Hee / Kim, Ikyon / Kim, Seong Hwan

    Archives of pharmacal research

    2017  Volume 40, Issue 11, Page(s) 1328–1335

    Abstract: ... skeletal development in zebrafish. The combination of BMP-2 with small molecules, including mollugin, could minimize ... its clinical limitations, and these molecules might lead to the development of effective stem cell stimulants ... for bone regeneration and fracture healing. ...

    Abstract Bone morphogenetic protein 2 (BMP-2) has been used clinically to encourage bone regeneration; although, there can be major side effects with larger doses. Therefore, there is a need to identify new small molecules to potentiate the osteogenic action of BMP-2. In this study, we investigated the effect of mollugin on bone formation in murine bi-potential mesenchymal progenitor C2C12 cells by combination with BMP-2. We found mollugin could enhance the BMP-2-mediated osteoblast differentiation of C2C12 cells. This was accompanied by the induction of other osteogenic BMPs. We also found the enhancing potential of mollugin may involve activation of the p38-Smad1/5/8 signaling axis. Furthermore, mollugin promoted skeletal development in zebrafish. The combination of BMP-2 with small molecules, including mollugin, could minimize its clinical limitations, and these molecules might lead to the development of effective stem cell stimulants for bone regeneration and fracture healing.
    MeSH term(s) Animals ; Bone Morphogenetic Protein 2/administration & dosage ; Bone Morphogenetic Protein 2/pharmacology ; Cell Differentiation/drug effects ; Cell Line ; Drug Therapy, Combination ; Humans ; Mesenchymal Stromal Cells/drug effects ; Mesenchymal Stromal Cells/metabolism ; Mice ; Osteoblasts/drug effects ; Osteoblasts/metabolism ; Osteogenesis/drug effects ; Pyrans/administration & dosage ; Pyrans/pharmacology ; Signal Transduction/drug effects ; Smad1 Protein/metabolism ; Smad5 Protein/metabolism ; Smad8 Protein/metabolism ; Zebrafish ; p38 Mitogen-Activated Protein Kinases/metabolism
    Chemical Substances BMP2 protein, human ; Bone Morphogenetic Protein 2 ; Pyrans ; Smad1 Protein ; Smad1 protein, mouse ; Smad5 Protein ; Smad5 protein, mouse ; Smad8 Protein ; Smad9 protein, mouse ; rubimaillin (55481-88-4) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2017-11
    Publishing country Korea (South)
    Document type Journal Article
    ZDB-ID 447623-2
    ISSN 1976-3786 ; 0253-6269
    ISSN (online) 1976-3786
    ISSN 0253-6269
    DOI 10.1007/s12272-017-0964-4
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    Zs.B 3229: Show issues Location:
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  4. Article: Mollugin enhances the osteogenic action of BMP-2 via the p38–Smad signaling pathway

    Moon, Seong-Hee / Ikyon Kim / Seong Hwan Kim

    Archives of pharmacal research. 2017 Nov., v. 40, no. 11

    2017  

    Abstract: ... skeletal development in zebrafish. The combination of BMP-2 with small molecules, including mollugin, could minimize ... its clinical limitations, and these molecules might lead to the development of effective stem cell stimulants ... for bone regeneration and fracture healing. ...

    Abstract Bone morphogenetic protein 2 (BMP-2) has been used clinically to encourage bone regeneration; although, there can be major side effects with larger doses. Therefore, there is a need to identify new small molecules to potentiate the osteogenic action of BMP-2. In this study, we investigated the effect of mollugin on bone formation in murine bi-potential mesenchymal progenitor C2C12 cells by combination with BMP-2. We found mollugin could enhance the BMP-2-mediated osteoblast differentiation of C2C12 cells. This was accompanied by the induction of other osteogenic BMPs. We also found the enhancing potential of mollugin may involve activation of the p38–Smad1/5/8 signaling axis. Furthermore, mollugin promoted skeletal development in zebrafish. The combination of BMP-2 with small molecules, including mollugin, could minimize its clinical limitations, and these molecules might lead to the development of effective stem cell stimulants for bone regeneration and fracture healing.
    Keywords Danio rerio ; adverse effects ; bone formation ; bone morphogenetic proteins ; mice ; osteoblasts ; signal transduction ; skeletal development ; stem cells
    Language English
    Dates of publication 2017-11
    Size p. 1328-1335.
    Publishing place Pharmaceutical Society of Korea
    Document type Article
    ZDB-ID 447623-2
    ISSN 1976-3786 ; 0253-6269
    ISSN (online) 1976-3786
    ISSN 0253-6269
    DOI 10.1007/s12272-017-0964-4
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    In stock of ZB MED Cologne/Königswinter

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  5. Article ; Online: Strontium attenuates rhBMP-2-induced osteogenic differentiation via formation of Sr-rhBMP-2 complex and suppression of Smad-dependent signaling pathway.

    Zhang, Wenjing / Tian, Yu / He, Hongyan / Chen, Rui / Ma, Yifan / Guo, Han / Yuan, Yuan / Liu, Changsheng

    Acta biomaterialia

    2016  Volume 33, Page(s) 290–300

    Abstract: ... of BMP/Smad signaling pathway, providing guidance for development of Sr-containing BMP-2-based bone ... BMPRIA and thus attenuated Smad 1/5/8 phosphorylation without affecting their dephosphorylation in C2C12 ... inhibiting bone resorption in bone regeneration. In this current study, the effect and the underlying mechanism involved ...

    Abstract Strontium (Sr(2+)) has pronounced effects on stimulating bone formation and inhibiting bone resorption in bone regeneration. In this current study, the effect and the underlying mechanism involved of Sr(2+) on the biological activity of bone morphogenetic protein-2 (BMP-2) were studied in detail with pluripotent skeletal muscle myogenic progenitor C2C12 model cell line. The results indicated that Sr(2+) could bind recombinant human BMP-2 (rhBMP-2) rapidly, even in the presence of Ca(2+) and Mg(2+), and inhibited rhBMP-2-induced osteogenic differentiation in vitro and osteogenetic efficiency in vivo. Further studies demonstrated that Sr(2+) treatment undermined the binding capacity of rhBMP-2 with its receptor BMPRIA and thus attenuated Smad 1/5/8 phosphorylation without affecting their dephosphorylation in C2C12 cells. Furthermore, circular dichroism spectroscopy, fluorescence spectroscopy and X-ray photoelectron spectroscopy all revealed that the inhibitory effect of Sr(2+) on the rhBMP-2 osteogenic activity was associated with the formation of Sr-rhBMP-2 complex and ensuing enhancement of β-sheet structure. Our work suggests the activity of rhBMP-2 to induce osteogenic differentiation was decreased by directly interaction with free Sr ions in solution, which should provide guide and assist for development of BMP-2-based materials for bone regeneration.
    Statement of significance: Due to easy denaturation and ensuing the reduced activity of rhBMP-2, preserving/enhancing the capacity of rhBMP-2 to induce osteogenic differentiation is of critical importance in developing the protein-based therapy. Cations as effective elements influence the conformation and thereby the bioactivity of protein. Strontium (Sr(2+)), stimulating bone formation and inhibiting bone resorption, has been incorporated into biomaterials/scaffold to improve the bioactivity for bone-regeneration applications. However, Sr(2+)-induced changes in the conformation and bioactivity of BMP-2 have never been investigated. In this study, the formation of Sr-rhBMP-2 complex inhibited the osteogenic differentiation in vitro and osteogenetic efficiency in vivo through the inhibition of BMP/Smad signaling pathway, providing guidance for development of Sr-containing BMP-2-based bone scaffold/matrice and other Sr-dopped protein therapy.
    MeSH term(s) Animals ; Blotting, Western ; Bone Morphogenetic Protein 2/chemistry ; Bone Morphogenetic Protein 2/pharmacology ; Bone Morphogenetic Protein Receptors/metabolism ; Cell Differentiation/drug effects ; Cell Line ; Cell Membrane/drug effects ; Cell Membrane/metabolism ; Choristoma/pathology ; Humans ; Ions ; Mice ; Models, Biological ; Osteogenesis/drug effects ; Protein Structure, Secondary ; Recombinant Proteins/chemistry ; Recombinant Proteins/pharmacology ; Signal Transduction/drug effects ; Smad Proteins/metabolism ; Strontium/pharmacology ; Thermodynamics ; Transforming Growth Factor beta/chemistry ; Transforming Growth Factor beta/pharmacology
    Chemical Substances Bone Morphogenetic Protein 2 ; Ions ; Recombinant Proteins ; Smad Proteins ; Transforming Growth Factor beta ; recombinant human bone morphogenetic protein-2 ; Bone Morphogenetic Protein Receptors (EC 2.7.11.30) ; Strontium (YZS2RPE8LE)
    Language English
    Publishing date 2016-01-29
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2173841-5
    ISSN 1878-7568 ; 1742-7061
    ISSN (online) 1878-7568
    ISSN 1742-7061
    DOI 10.1016/j.actbio.2016.01.042
    Database MEDical Literature Analysis and Retrieval System OnLINE

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