Mesenchymal stem cells (MSCs) have the potential to differentiate into neuron-like cells, which may provide a new strategy for the clinical treatment of neurodegenerative diseases such as Parkinson's disease (PD). However, the application of MSCs in the patients is still limited as the reason of efficiency and safety of transplantation. The aim of this study is to develop a new method and induce human umbilical cord MSCs (hUCMSCs) into neuron-like cells. Results from flow cytometry indicate that the isolated MSCs from hUCMSCs exhibited a typical phenotype of adult stem cells and express CD44, CD54, CD73, CD90, CD105, CD166, and HLA-ABC. Furthermore, the induced cells from hUCMSCs could spontaneously express different neural cell markers [neuron-specific enolase (NSE) and glial fibrillary acidic protein (GFAP)], even transcription factors related to dopaminergic neuron's development (Nurr1, Wnt-1, and En-1). Moreover, after treatment of EHFBT (extracts of human fetal brain tissue), hUCMSCs can express neuronal markers such as Nestin, LIM homeobox transcription factor 1 beta (LMX1B), dopamine beta hydroxylase (DBH), and dopamine transporter (DAT). In summary, a method that can induce hUCMSCs into dopaminergic neuron containing cells is established by the treatment of EHFBT. This would provide us a new cell source for PD in clinical treatment in the future.
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http://dx.doi.org/10.1089/cell.2020.0029 | DOI Listing |
Exp Hematol Oncol
January 2025
Department of Hematology, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Myelodysplastic Syndromes (MDS) represent a group of heterogeneous myeloid clonal diseases derived from aberrant hematopoietic stem/progenitor cells. Enhancer of zeste homolog 2 (EZH2) is an important regulator in gene expression through methyltransferase-dependent or methyltransferase-independent mechanisms. Herein, we found EZH2 inhibition led to MDS cell pyroptosis through RNA Helicase A (RHA) down-regulation induced overexpression of S100A9, a key regulator of inflammasome activation and pyroptosis.
View Article and Find Full Text PDFBioelectron Med
January 2025
School of Pharmacy, Biodiscovery Institute & Boots Science Building, University of Nottingham, Nottingham, NG7 2RD, UK.
Background: In glioblastoma (GBM) therapy research, tumour treating fields by the company Novocure™, have shown promise for increasing patient overall survival. When used with the chemotherapeutic agent temozolomide, they extend median survival by five months. However, there is a space to design alternative systems that will be amenable for wider use in current research.
View Article and Find Full Text PDFStem Cell Res Ther
January 2025
Department of Neurosurgery, The First Medical Centre, Chinese PLA General Hospital, Beijing, 100853, China.
Background: Closed head injury (CHI) provokes a prominent neuroinflammation that may lead to long-term health consequences. Microglia plays pivotal and complex roles in neuroinflammation-mediated neuronal insult and repair following CHI. We previously reported that induced neural stem cells (iNSCs) can block the effects of CXCL12/CXCR4 signaling on NF-κB activation in activated microglia by CXCR4 overexpression.
View Article and Find Full Text PDFActa Neuropathol Commun
January 2025
Department of Physiology and Pharmacology, Sapienza University of Rome, 00185, Rome, Italy.
The generation of retinal models from human induced pluripotent stem cells holds significant potential for advancing our understanding of retinal development, neurodegeneration, and the in vitro modeling of neurodegenerative disorders. The retina, as an accessible part of the central nervous system, offers a unique window into these processes, making it invaluable for both study and early diagnosis. This study investigates the impact of the Frontotemporal Dementia-linked IVS 10 + 16 MAPT mutation on retinal development and function using 2D and 3D retinal models derived from human induced pluripotent stem cells.
View Article and Find Full Text PDFJ Orthop Surg Res
January 2025
Department of Joint Osteopathy, Liuzhou Worker's Hospital, Liuzhou, Guangxi Province, 545000, China.
Alcoholic osteonecrosis of the femoral head (AIONFH) is caused by long-term heavy drinking, which leads to abnormal alcohol and lipid metabolism, resulting in femoral head tissue damage, and then pathological necrosis of femoral head tissue. If not treated in time in clinical practice, it will seriously affect the quality of life of patients and even require hip replacement to treat alcoholic femoral head necrosis. This study will confirm whether M2 macrophage exosome (M2-Exo) miR-122 mediates alcohol-induced BMSCs osteogenic differentiation, ultimately leading to the inhibition of femoral head necrosis.
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