Interleukin 15 participates in Jagged1-induced mineralization in human dental pulp cells

Kornsuthisopon, Chatvadee; Manokawinchoke, Jeeranan; Sonpoung, Opor; Osathanon, Thanaphum; Damrongsri, Damrong

doi:10.1016/j.archoralbio.2021.105163

Cited by 4 publications

(3 citation statements)

References 43 publications

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“…Additionally, immobilization of JAG1 induced odonto/ osteogenic differentiation in human pulp cells (hDPs) suggests its potential role in reparative dentin formation (Manokawinchoke et al, 2017;Manaspon et al, 2020). In another study that further confirms the role of JAG1 in hDP differentiation, Kornsuthisopon et al (2021) described the participation of the cytokine IL-15 in JAG1-induced mineralization in hDPs. The study demonstrated that cells treated with JAG1 resulted in the upregulation of IL-15 and IL-15RA mRNA expression and cells treated with IL-15 resulted in a significant increase in mineral deposition.…”

Section: Clinical Applications Of Jag1mentioning

confidence: 91%

Biomedical engineering approaches for the delivery of JAGGED1 as a potential tissue regenerative therapy

Kaimari,

Kamalakar,

Goudy

2023

Front. Bioeng. Biotechnol.

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JAG1 is a ligand that activates the NOTCH signaling pathway which plays a crucial role in determining cell fate behavior through cell-to-cell signaling. JAG1-NOTCH signaling is required for mesenchymal stem cell (MSC) differentiation into cardiomyocytes and cranial neural crest (CNC) cells differentiation into osteoblasts, making it a regenerative candidate for clinical therapy to treat craniofacial bone loss and myocardial infarction. However, delivery of soluble JAG1 has been found to inhibit NOTCH signaling due to the requirement of JAG1 presentation in a bound form. For JAG1-NOTCH signaling to occur, JAG1 must be immobilized within a scaffold and the correct orientation between the NOTCH receptor and JAG1 must be achieved. The lack of clinically translatable JAG1 delivery methods has driven the exploration of alternative immobilization approaches. This review discusses the role of JAG1 in disease, the clinical role of JAG1 as a treatment, and summarizes current approaches for JAG1 delivery. An in-depth review was conducted on literature that used both in vivo and in vitro delivery models and observed the canonical versus non-canonical NOTCH pathway activated by JAG1. Studies were then compared and evaluated based on delivery success, functional outcomes, and translatability. Delivering JAG1 to harness its ability to control cell fate has the potential to serve as a therapeutic for many diseases.

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Section: Clinical Applications Of Jag1mentioning

confidence: 91%

Biomedical engineering approaches for the delivery of JAGGED1 as a potential tissue regenerative therapy

Kaimari,

Kamalakar,

Goudy

2023

Front. Bioeng. Biotechnol.

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“…In addition, it regulates the glucose uptake and fatty acid oxidation in skeletal muscle 72 . Since IL‐15 is a potential proinflammatory cytokine that is expressed at high levels under inflammatory conditions in both muscle and bone, this myokine may be considered another muscle‐derived mediator of bone erosion and bone loss in orthopedic inflammatory diseases such as rheumatoid arthritis and periodontal disease 73,74 …”

Section: Clinical Challengementioning

confidence: 99%

The critical impact of traumatic muscle loss on fracture healing: Basic science and clinical aspects

Rahmati,

Haffner,

Lee

et al. 2023

Journal Orthopaedic Research

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Musculoskeletal trauma, specifically fractures, is a leading cause of patient morbidity and disability worldwide. In approximately 20% of cases with fracture and related traumatic muscle loss, bone healing is impaired leading to fracture nonunion. Over the past few years, several studies have demonstrated that bone and the surrounding muscle tissue interact not only anatomically and mechanically but also through biochemical pathways and mediators. Severe damage to the surrounding musculature at the fracture site causes an insufficiency in muscle‐derived osteoprogenitor cells that are crucial for fracture healing. As an endocrine tissue, skeletal muscle produces many myokines that act on different bone cells, such as osteoblasts, osteoclasts, osteocytes, and mesenchymal stem cells. Investigating how muscle influences fracture healing at cellular, molecular, and hormonal levels provides translational therapeutic solutions to this clinical challenge. This review provides an overview about the contributions of surrounding muscle tissue in directing fracture healing. The focus of the review is on describing the interactions between bone and muscle in both healthy and fractured environments. We discuss current progress in identifying the bone–muscle molecular pathways and strategies to harness these pathways as cues for accelerating fracture healing. In addition, we review the existing challenges and research opportunities in the field.

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“…The previous report demonstrated that IWP-2 at 25 μM effectively blocked Wnt pathway and was able to inhibit Jagged1-induced mineralization in hDPSCs (Kornsuthisopon, Chansaenroj, et al, 2022). We varied the IWP-2 concentration and performed the MTT assay to assess cell viability and proliferation.…”

Section: Iwp-2 At 25 μM Concentration Has No Effect On Cell Viability...mentioning

confidence: 99%

IWP‐2 modulates the immunomodulatory properties of human dental pulp stem cells in vitro

Chansaenroj,

Kornsuthisopon,

Suwittayarak

et al. 2023

Int Endodontic J

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AimTo investigate the effect of IWP‐2, Wnt inhibitor, on human dental pulp stem cells (hDPSCs) responses.MethodologyhDPSCs were isolated from human dental pulp tissues. Cells were treated with 25 μM IWP‐2 for 24 h, and subsequently, the gene expression profile was examined using high‐throughput RNA sequencing. The mRNA expression was analysed using qPCR. The effect of IWP‐2 was investigated in both normal and LPS‐induced hDPSCs (inflamed hDPSCs). CD4+ T cells and CD14+ monocyte‐derived macrophages were cultured with conditioned media of IWP‐2 treated hDPSCs to observe the immunosuppressive property.ResultsRNA sequencing indicated that IWP‐2 significantly downregulated several KEGG pathways, including cytokine‐cytokine receptor interaction, IL‐17 signalling pathway, and TNF signalling pathway. In both normal and inflamed conditions, IWP‐2 markedly upregulated TGFB1 mRNA expression while the mRNA expression of pro‐inflammatory cytokines, TNFA, IL1B, IFNG, and IL6, was inhibited. In the inhibition experiment, the pretreatment with p38, MAPK, or PI3K inhibitors abolished the effects of IWP‐2 in LPS‐induced inflammation. In terms of immune cells, IWP‐2‐treated‐inflamed hDPSCs conditioned media attenuated T cell proliferation and regulated regulatory T cell differentiation. In addition, the migratory property of macrophage was decreased after being exposed to IWP‐2‐treated inflamed hDPSCs conditioned media.ConclusionIWP‐2 suppressed inflammatory cytokine expression in both normal and inflamed hDPSCs. Moreover, hDPSCs exerted the immunosuppressive property after IWP‐2 treatment. These results suggest the role of Wnt in inflammatory responses and immunomodulation in dental pulp tissues.

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Interleukin 15 participates in Jagged1-induced mineralization in human dental pulp cells

Cited by 4 publications

References 43 publications

Biomedical engineering approaches for the delivery of JAGGED1 as a potential tissue regenerative therapy

Biomedical engineering approaches for the delivery of JAGGED1 as a potential tissue regenerative therapy

The critical impact of traumatic muscle loss on fracture healing: Basic science and clinical aspects

IWP‐2 modulates the immunomodulatory properties of human dental pulp stem cells in vitro

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