Additional file 3 of Inflammatory stimulation of astrocytes affects the expression of miRNA-22-3p within NSCs-EVs regulating remyelination by targeting KDM3A

Additional file 3. Figure S3: LPS-As-CM addition significantly upregulated the expression of miRNA-22 within NSC-EVs, which could inhibit the expression of KDM3A in NSCs. A. the expressions of axon-related and remyelination-related miRNAs within As-NSC-EVs and LPS-As-NSC-EVs were detected by PCR (n = 3; data are the mean ± S.D.; *p 0.05). B. the expression of the predicted genes was detected in NSCs by PCR with or without transfection of the miRNA-22 mimics (n = 3; data are the mean ± S.D.; *p 0.05). C. Dual luciferase reporter analysis showed that the luciferase activity was not altered by the transfection of miRNA-22 mimics in the HOMER1 and TGFBR1 groups (n = 3; data are the mean ± S.D.; *p 0.05)

Additional file 2 of Inflammatory stimulation of astrocytes affects the expression of miRNA-22-3p within NSCs-EVs regulating remyelination by targeting KDM3A

Additional file 2. Figure S2: The full-length of original gels

Additional file 1 of Inflammatory stimulation of astrocytes affects the expression of miRNA-22-3p within NSCs-EVs regulating remyelination by targeting KDM3A

Additional file 1.Figure S1: A. Identification of BMSC-EVs by transmission electron microscopy. B. Analysis of CD9, CD63, and TSG101 expression by western blot C. Detection of the diameter of BMSC-EVs by dynamic light scattering

Data_Sheet_1_Micro-RNA let-7a-5p Derived From Mesenchymal Stem Cell-Derived Extracellular Vesicles Promotes the Regrowth of Neurons in Spinal-Cord-Injured Rats by Targeting the HMGA2/SMAD2 Axis.docx

Spinal cord injury (SCI) often causes neuronal and axonal damage, resulting in permanent neurological impairments. Mesenchymal stem cells (MSCs) and extracellular vesicles (EVs) are promising treatments for SCI. However, the underlying mechanisms remain unclear. Herein, we demonstrated that EVs from bone marrow-derived MSCs promoted the differentiation of neural stem cells (NSCs) into the neurons and outgrowth of neurites that are extending into astrocytic scars in SCI rats. Further study found that let-7a-5p exerted a similar biological effect as MSC-EVs in regulating the differentiation of NSCs and leading to neurological improvement in SCI rats. Moreover, these MSC-EV-induced effects were attenuated by let-7a-5p inhibitors/antagomirs. When investigating the mechanism, bioinformatics predictions combined with western blot and RT-PCR analyses showed that both MSC-EVs and let-7a-5p were able to downregulate the expression of SMAD2 by inhibiting HMGA2. In conclusion, MSC-EV-secreted let-7a-5p promoted the regrowth of neurons and improved neurological recovery in SCI rats by targeting the HMGA2/SMAD2 axis.</p