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  • Wang, Zilu  (3)
  • 1
    Online Resource
    Online Resource
    Springer Science and Business Media LLC ; 2016
    In:  Scientific Reports Vol. 6, No. 1 ( 2016-11-11)
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 6, No. 1 ( 2016-11-11)
    Abstract: Insulin-like growth factor-1 (IGF-1) and its receptor IGF-1R play a paramount role in tooth/bone formation while hsa-let-7c actively participates in the osteogenic differentiation of mesenchymal stem cells. However, the interaction between IGF-1/IGF-1R and hsa-let-7c on the committed differentiation of stem cells from apical papilla (SCAPs) remains unclear. In this study, human SCAPs were isolated and treated with IGF-1 and hsa-let-7c over/low-expression viruses. The odonto/osteogenic differentiation of these stem cells and the involvement of mitogen-activated protein kinase (MAPK) pathway were subsequently investigated. Alizarin red staining showed that hsa-let-7c low-expression can significantly promote the mineralization of IGF-1 treated SCAPs, while hsa-let-7c over-expression can decrease the calcium deposition of IGF-1 treated SCAPs. Western blot assay and real-time reverse transcription polymerase chain reaction further demonstrated that the expression of odonto/osteogenic markers (ALP, RUNX2/ RUNX2 , OSX/ OSX , OCN/ OCN , COL-I/ COL-I , DSPP/ DSP , and DMP-1/ DMP-1 ) in IGF-1 treated SCAPs were significantly upregulated in Let-7c -low group. On the contrary, hsa-let-7c over-expression could downregulate the expression of these odonto/osteogenic markers. Moreover, western blot assay showed that the JNK and p38 MAPK signaling pathways were activated in Let-7c -low SCAPs but inhibited in Let-7c -over SCAPs. Together, the IGF-1/IGF-1R/ hsa-let-7c axis can control the odonto/osteogenic differentiation of IGF-1-treated SCAPs via the regulation of JNK and p38 MAPK signaling pathways.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2016
    detail.hit.zdb_id: 2615211-3
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  • 2
    In: Stem Cell Research & Therapy, Springer Science and Business Media LLC, Vol. 5, No. 6 ( 2014-12)
    Type of Medium: Online Resource
    ISSN: 1757-6512
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2014
    detail.hit.zdb_id: 2548671-8
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  • 3
    In: BioMed Research International, Hindawi Limited, Vol. 2014 ( 2014), p. 1-12
    Abstract: Background Information . NF- κ B signaling pathway plays a complicated role in the biological functions of mesenchymal stem cells. However, the effects of NF- κ B pathway on the odonto/osteogenic differentiation of stem cells from apical papilla (SCAPs) remain unclear. The present study was designed to evaluate the effects of canonical NF- κ B pathway on the osteo/odontogenic capacity of SCAPs in vitro . Results . Western blot results demonstrated that NF- κ B pathway in SCAPs was successfully activated by TNF- α or blocked by BMS-345541. NF- κ B pathway-activated SCAPs presented a higher proliferation activity compared with control groups, as indicated by dimethyl-thiazol-diphenyl tetrazolium bromide assay (MTT) and flow cytometry assay (FCM). Wound scratch assay revealed that NF- κ B pathway-activated SCAPs presented an improved migration capacity, enhanced alkaline phosphatase (ALP) activity, and upregulated mineralization capacity of SCAPs, as compared with control groups. Meanwhile, the odonto/osteogenic markers ( ALP /ALP, RUNX2 /RUNX2, OSX /OSX, OCN /OCN, OPN /OPN, BSP /BSP, DSPP /DSP, and DMP-1 /DMP-1) in NF- κ B pathway-activated SCAPs were also significantly upregulated as compared with control groups at both protein and mRNA levels. However, NF- κ B pathway-inhibited SCAPs exhibited a lower proliferation/migration capacity, and decreased odonto/osteogenic ability in comparison with control groups. Conclusion . Our findings suggest that classical NF- κ B pathway plays a paramount role in the proliferation and committed differentiation of SCAPs.
    Type of Medium: Online Resource
    ISSN: 2314-6133 , 2314-6141
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2014
    detail.hit.zdb_id: 2698540-8
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