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Uncovering mechanisms of endogenous regeneration and repair through resident stem cell activation will allow us to develop specific therapies for injuries and diseases by targeting resident stem cell lineages. Sox9+ stem cells have been reported to play an essential role in acute kidney injury (AKI). However, a complete view of the Sox9+ lineage was not well investigated to accurately elucidate the functional end state and the choice of cell fate during tissue repair after AKI. To identify the mechanisms of fate determination of Sox9+ stem cells, we set up an AKI model with prostaglandin E2 (PGE2) treatment in a Sox9 lineage tracing mouse model. Single‐cell RNA sequencing (scRNA‐seq) was performed to analyse the transcriptomic profile of the Sox9+ lineage. Our results revealed that PGE2 could activate renal Sox9+ cells and promote the differentiation of Sox9+ cells into renal proximal tubular epithelial cells and inhibit the development of fibrosis. Furthermore, single‐cell transcriptome analysis demonstrated that PGE2 could regulate the restoration of lipid metabolism homeostasis in proximal tubular epithelial cells by participating in communication with different cell types. Our results highlight the prospects for the activation of endogenous renal Sox9+ stem cells with PGE2 for the regenerative therapy of AKI. [ABSTRACT FROM AUTHOR]

A recent article in Global Medical Genetics discusses the use of mesenchymal stem cells (MSCs) in clinical trials for immune disorders. MSCs have unique properties, including regeneration and immunomodulation, which make them a promising therapeutic approach. The article highlights a phase I trial that used human umbilical cord-derived MSCs (UC-MSCs) to treat refractory immune thrombocytopenia (ITP), a hemorrhagic disease resulting from an immune imbalance. The trial showed that UC-MSCs increased platelet counts and improved bleeding symptoms in patients with refractory ITP. MSCs have the potential to treat various immune-related conditions, and further research is needed to understand their distribution and metabolism in organ tissues. [Extracted from the article]

Previous studies have highlighted the antitumor effects of mesenchymal stem cell-derived extracellular vesicles (MSC-EVs), positioning them as a promising therapeutic avenue for cancer treatment. However, some researchers have proposed a bidirectional influence of MSC-EVs on tumors, determined by the specific tissue origin of the MSCs and the types of tumors involved. The present study aimed to elucidate the effects of human placenta MSC-derived extracellular vesicles (hPMSC-EVs) on the malignant behavior of a mouse breast cancer model of 4T1 cells in vitro and in vivo. The findings revealed that hPMSC-EVs significantly inhibited the proliferation, migration and colony formation of cultured 4T1 mouse breast cancer cells without inducing apoptosis. Exposure to conditioned medium from 4T1 cells pretreated with hPMSC-EVs resulted in decreased angiogenic activity, accompanied by the downregulation of angiogenesis-promoting genes in human umbilical vein endothelial cells. In murine xenograft models derived from the 4T1 cell line, local administration of hPMSC-EVs substantially hindered tumor growth. Further results revealed that hPMSC-EVs inhibited angiogenesis in vivo, as reflected by the use of a vascular growth factor receptor 2-Fluc transgenic mouse model. In summary, the results confirmed that hPMSC-EVs negatively modulated breast cancer growth by suppressing tumor cell proliferation and migration via an indirect antiangiogenic mechanism. These results underscored the therapeutic potential of EVs, suggesting a promising avenue for alternative anticancer treatments in the future. [ABSTRACT FROM AUTHOR]