Transplanted adipose stem cells (ASC) have a low survival rate in the body, and there are not many ASC that can be effectively used, which weakens their tissue repair function. Based on this status quo, a new type of copper-based metal-organic network (Cu-MON) was used to pretreat cells to regulate cell activity in order to improve the efficacy of cell therapy or reduce the number of cells used, thus reducing the cost of clinical treatment. Gene expression changes before and after Cu-MON treatment of normal donor adipose stem cells (ND-ASC) and type 2 diabetes mellitus adipose stem cells (T2DM-ASC) were evaluated through RNA sequencing, KEGG and GO enrichment analysis. The results showed that Cu-MON improved ASC cell quality by regulating immune response and promoting paracrine secretion. IL-17 signaling pathway and IL-6, CXCL8, and MMP-9 were key pathways and necessary genes that affected the ability of stem cells. In addition, Cu-MON also improved stem cell antiviral ability through Type I interferon signaling pathway. Our research showed that Cu-MON had improved the cell quality of ASC by regulating immune response, promoting paracrine secretion, and improving antiviral capabilities. This approach to biomaterial pretreatment is fast, convenient, and relatively safe, and provides new strategies for improving the efficiency of cell therapies.
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http://dx.doi.org/10.1096/fba.2024-00153 | DOI Listing |
PLoS One
March 2025
Department of Hematology, Heping Hospital Affiliated to Changzhi Medical College, Changzhi Medical College, Changzhi, Shanxi, China.
Objective: This study aims to investigate and analyze the differentially expressed genes (DEGs) in CD34 + hematopoietic stem cells (HSCs) from patients with myelodysplastic syndromes (MDS) through bioinformatics analysis, with the ultimate goal of uncovering the potential molecular mechanisms underlying pathogenesis of MDS. The findings of this study are expected to provide novel insights into clinical treatment strategies for MDS.
Methods: Initially, we downloaded three datasets, GSE81173, GSE4619, and GSE58831, from the public Gene Expression Omnibus (GEO) database as our training sets, and selected the GSE19429 dataset as the validation set.
Proc Natl Acad Sci U S A
March 2025
Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Hokkaido 060-0815, Japan.
Currently, most cell or tissue transplantations using induced pluripotent stem cells (iPSCs) are anticipated to involve allogeneic iPSCs. However, the immunological properties of iPSCs in an allogeneic setting are not well understood. We previously established a mouse transplantation model of MHC-compatible/minor antigen-mismatched combinations, assuming a hypoimmunogenic iPSC-setting.
View Article and Find Full Text PDFSTAR Protoc
March 2025
Unidad de Regeneración Neural, Unidad Funcional de Investigación de Enfermedades Crónicas (UFIEC), Instituto de Salud Carlos III (ISCIII), Majadahonda, Madrid 28220, Spain. Electronic address:
Human cerebral organoids (hCOs) provide an excellent model for the study of human brain development and disease. Here, we present a protocol to obtain hCOs directly from two-dimensional (2D) pluripotent stem cell (PSC) cultures, avoiding cell dissociation and posterior embryoid body (EB) aggregation. We describe steps for subjecting 2D cultures to a neural fate and subsequently developing hCOs.
View Article and Find Full Text PDFCell Rep
March 2025
Department of Biomedicine, Aarhus University, 8000 Aarhus, Denmark. Electronic address:
Plasmacytoid dendritic cells (pDCs) play a pivotal role in immune responses, particularly against viral infections. pDCs exhibit diverse functions, including interferon production, cytokine secretion, and antigen presentation. Here, we investigate the antigen cross-presentation capacity of pDCs and their role in CD8 T cell activation.
View Article and Find Full Text PDFAm J Physiol Endocrinol Metab
March 2025
Department of Kinesiology, East Carolina University, Greenville, North Carolina, United States.
Offspring exposed to metformin treatment for gestational diabetes mellitus (GDM) experience altered growth patterns that increase the risk for developing cardiometabolic diseases later in life. The adaptive cellular mechanisms underlying these patterns remain unclear. Therefore, the objective of this study was to determine if chronic metformin exposure associated with GDM treatment elicits infant cellular metabolic adaptations.
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