Abstract
Inflammation is a common feature of many neurodegenerative diseases. The treatment of stem cells as a therapeutic approach to repair damage in the central nervous system represents a valid alternative. In this study, using Next-Generation Sequencing (NGS) technology, we analyzed the transcriptomic profile of human Gingival Mesenchymal Stem Cells (hGMSCs) treated with Moringin [4-(α-l-ramanosyloxy)-benzyl isothiocyanate] (hGMSCs-MOR) or with Cannabidiol (hGMSCs-CBD) at dose of 0.5 or 5 µM, respectively. Moreover, we compared their transcriptomic profiles in order to evaluate analogies and differences in pro- and anti-inflammatory pathways. The hGMSCs-MOR selectively downregulate TNF-α signaling from the beginning, reducing the expression of TNF-α receptor while hGMSCs-CBD limit its activity after the process started. The treatment with CBD downregulates the pro-inflammatory pathway mediated by the IL-1 family, including its receptor while MOR is less efficient. Furthermore, both the treatments are efficient in the IL-6 signaling. In particular, CBD reduces the effect of the pro-inflammatory JAK/STAT pathway while MOR enhances the pro-survival PI3K/AKT/mTOR. In addition, both hGMSCs-MOR and hGMSCs-CBD improve the anti-inflammatory activity enhancing the TGF-β pathway.
Keywords:
Cannabidiol; Moringin; human gingival mesenchymal stem cells; inflammation; transcriptome analysis.
MeSH terms
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Anti-Inflammatory Agents / pharmacology*
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Cannabidiol / pharmacology*
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Gene Expression Profiling
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Gene Expression Regulation
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Gingiva / cytology
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Gingiva / drug effects
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Gingiva / immunology
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Humans
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Interleukin-1 / genetics
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Interleukin-1 / immunology
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Interleukin-6 / genetics
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Interleukin-6 / immunology
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Isothiocyanates / pharmacology*
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Janus Kinases / genetics
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Janus Kinases / immunology
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Mesenchymal Stem Cells / cytology
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Mesenchymal Stem Cells / drug effects*
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Mesenchymal Stem Cells / immunology
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Phosphatidylinositol 3-Kinases / genetics
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Phosphatidylinositol 3-Kinases / immunology
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Primary Cell Culture
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Proto-Oncogene Proteins c-akt / genetics
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Proto-Oncogene Proteins c-akt / immunology
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Receptors, Interleukin-1 / genetics
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Receptors, Interleukin-1 / immunology
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STAT Transcription Factors / genetics
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STAT Transcription Factors / immunology
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Signal Transduction / drug effects*
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Signal Transduction / genetics
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Signal Transduction / immunology
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TOR Serine-Threonine Kinases / genetics
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TOR Serine-Threonine Kinases / immunology
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Transcriptome / drug effects*
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Transcriptome / immunology
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Transforming Growth Factor beta / genetics
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Transforming Growth Factor beta / immunology
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Tumor Necrosis Factor-alpha / genetics
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Tumor Necrosis Factor-alpha / immunology
Substances
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Anti-Inflammatory Agents
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IL6 protein, human
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Interleukin-1
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Interleukin-6
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Isothiocyanates
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Receptors, Interleukin-1
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STAT Transcription Factors
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Transforming Growth Factor beta
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Tumor Necrosis Factor-alpha
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moringin
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Cannabidiol
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MTOR protein, human
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Janus Kinases
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Proto-Oncogene Proteins c-akt
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TOR Serine-Threonine Kinases