Glioma is one of the malignancy brain tumors, which deeply threaten the health of patients. Although the traditional therapies for glioma have improved, the outcome is still far from satisfactory. Bone Marrow Stromal Cells (BMSC)-based therapy provided novel insight in the treatment for glioma. However, the detailed molecular mechanism is still not clear. The aim of present study is to discover the novel factor in BMSC-based therapy for glioma. The cell proliferation and apoptosis were identified by using CCK-8 and flow cytometry. The invasion of glioma cells was examined by using Transwell assay and wound-healing assay respectively. qRT-PCR was used to examine the expression of miR-506. Western blot was used to examine the protein levels of CD63, TSG101, NUR77 and CXCR4. Our data suggested that BMSC-derived exosome inhibited the proliferation and contributed to apoptosis of human U87 cells after culturing with miR-506 mimic. Overexpression of miR-506 in BMSC-derived exosome inhibited the invasion of human glioma U87 cells, while these effects were deeply suppressed in the presence GW4869. Our present study demonstrated that BMSC inhibited the growth and metastasis of human glioma U87 cells through delivering exosomal miR-506, and provided the evidences to develop the BMSC-based therapy for glioma.

Introduction: Diabetic nephropathy (DN) is a leading cause of end-stage kidney disease (ESKD), with renal fibrosis as a key pathological hallmark. However, the cellular and molecular drivers of fibrosis remain incompletely defined. Here, we employed singlecell RNA sequencing (scRNA-seq) to delineate pro-fibrotic cell subsets and their key regulatory factors in human DN kidneys, providing a higher-resolution view compared to previous fibrosis-related scRNA-seq studies. Methods: Publicly available scRNA-seq datasets from human DN and control kidneys were analyzed to identify fibrosis-associated fibroblast subsets. A Tmsb10-high fibroblast population was prioritized. Functional validation was performed through Tmsb10 knockdown in NIH-3T3 fibroblasts and in a diabetic mouse model, followed by assessment of fibrosis markers, extracellular matrix (ECM) deposition, and TGF-β/SMAD signaling. Results: scRNA-seq revealed a significant expansion of Tmsb10-high fibroblasts in DN kidneys, exhibiting strong enrichment of ECM-related and TGF-β/SMAD-responsive genes. Tmsb10 knockdown reduced Fn1, Col1a1, and α-Sma expression by approximately 50-70% and markedly attenuated ECM accumulation in vivo. Mechanistically, TMSB10 deficiency suppressed phosphorylation of SMAD2/3, mitigating fibroblast activation and matrix deposition. Discussion: This study identifies TMSB10 as a novel fibroblast-specific regulator of renal fibrosis in DN, acting through the TGF-β/ SMAD pathway. These findings expand current understanding of fibroblast heterogeneity and highlight TMSB10 as a potential therapeutic target for DN and other fibrotic diseases. Limitations include validation in a limited sample size and the use of murine fibroblast models, warranting further confirmation in human primary cells.