Background Pruritus is a recurring, long-lasting skin disease with few effective treatments. Many patients have unsatisfactory responses to currently available antipruritic treatments, and effective therapeutics are urgently needed to relieve symptoms. A previous study reported that mesenchymal stem cell (MSC)-mediated immune regulation could be used to treat skin inflammatory diseases. Multilineage-differentiating stress-enduring (Muse) cells are a new type of pluripotent stem cell that may also have the potential to treat inflammatory skin diseases. Methods Muse cells were isolated from human bone marrow-derived MSCs (BMSCs) via the 8-h longterm trypsin incubation (LTT) method. Repeated use of 2,4-dinitrofluorobenzene (DNFB) induced atopic dermatitis (AD) in a mouse model. Immunofluorescence, behavior recording, and image analysis were used to evaluate the therapeutic effect of subcutaneous Muse cell injection. Real-time quantitative polymerase chain reaction (qPCR) was used to measure the expression of inflammatory factors. In vitro, wound healing and cell proliferation experiments were used to examine the effect of Muse cell supernatant on keratinocytes. Results Our results showed that subcutaneous injection of Muse cells after AD model induction significantly alleviated scratching behavior in mice. The evaluation of dermatitis and photos of damaged skin on the back of the neck revealed that Muse cells reduced dermatitis, playing an active role in healing the damaged skin. The activation of spinal glial cells and scratching behavior were also reduced by Muse cell injection. In addition, we also showed that the expression levels of the inflammatory factors interleukin (IL)-6, IL-17α, and IL-33 in both the spinal cord and skin were suppressed by Muse cells. Furthermore, Muse cells not only exerted anti-inflammatory effects on lipopolysaccharide (LPS)-induced human HaCat cells but also promoted wound healing and keratinocyte proliferation. Conclusions In vivo, Muse cells could alleviate scratching symptoms, reduce epidermal inflammation, and promote wound healing. In vitro, Muse cells could also promote the migration and proliferation of keratinocytes. In summary, Muse cells may become a new therapeutic agent for the treatment of AD.
Clinical therapies for chronic pain are limited. While targeted drugs are promising therapies for chronic pain, they exhibit insufficient efficacy and poor targeting. The occurrence of chronic pain partly results from central changes caused by alterations in neurons in the rostral ventromedial medulla (RVM) in the brainstem regulatory pathway. The RVM, which plays a key role in the descending pain control pathway, greatly contributes to the development and maintenance of pain. However, the exact roles of the RVM in chronic pain remain unclear, making it difficult to develop new drugs targeting the RVM and related pathways. Here, we first discuss the roles of the RVM and related circuits in chronic pain. Then, we analyze synaptic transmission between RVM neurons and spinal cord neurons, specifically focusing on the release of neurotransmitters, to explore the cellular mechanisms by which the RVM regulates chronic pain. Finally, we propose some ideas for the development of drugs targeting the RVM.
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