Supporting data for "Role of STING in MSC senescence"
Reason: Unpublished Data
Supporting data for "Role of STING in MSC senescence"
This dataset contains raw data for the thesis "Role of STING in MSC senescence."
Mesenchymal stem cells (MSC) are a population of stem cells that possess a strong capacity for self-renewal, differentiation, and immunoregulation. Due to its easy accessibility and powerful potential, MSC has been considered a promising therapeutic reagent for various diseases. By 2020, there are more than 1000 clinical trials registered exploring the clinical application of MSC, and around 10 commercial MSC products have been approved. However, most of the clinical trials failed to meet the primary therapeutic end point in their late stage. Compromised therapeutic efficacy resulted from properties alteration and function loss of MSC can be induced by multiple factors in the process of MSC transplantation, including cellular senescence.
Cellular senescence is a process which elicits upon various insults, resulting in a series of alterations such as morphology changes, chromatin rearrangement and metabolic reprogramming. During senescence, cells could secret a wide range of cytokines, chemokines and proteinases termed senescence-associated secretory phenotype (SASP), which could pose an effect on the senescent cells and the microenvironment and accelerate the senescence process in turn. MSC senescence has been reported to be observed in those cells isolated from elder donors and harvested from long period expansion in vitro. In addition, MSCs can also grow senescence in inflammation environment, which may help explain the short duration of MSC after transplanted into recipients. Since the immunomodulatory properties of MSC are exerted through soluble mediators, the senescence of MSC can greatly impair its function in immunosuppression. Due to the prominent effect of MSC senescence on its function and therapeutic efficacy after transplantation, it is essential to monitor senescence and understand the underlying mechanism of this process.
Recent studies demonstrated that STING pathway was activated during senescence, mediating the type I interferon secretion and SASP response. However, most of the experiments were performed in MEF cells or fibroblast cells. Thus, we aimed to explore the role of STING pathway in MSC senescence and how this process may contribute to improve the therapeutic efficacy of MSCs transplantation.
This dataset consists of the results of the experiments involved in this thesis, including Western Blotting, Immunofluorescence staining, MTT assay, SA-β-gal staining, and flow cytometry. All mice models and results were included.