We have treated undifferentiated mouse embryonic stem (ES) cells with all-trans retinoic acid (RA) to induce differentiation in vitro into neuron-like cells with good cell viability for use as a graft. Furthermore, we asked whether the RA-induced neuron-like cells restored neurological dysfunction. To this end, the cells were transplanted into right hemiplegia model of mice, developed by a cryogenic injury of motor cortex. Motor function of the recipients was gradually improved, whereas little improvement was observed in control mice. The lesion showed clustering of mature and almost mature neuron-like cells in mice transplanted with the RA-treated cells. The grafted cells had synaptic vesicles. This finding may suggest their maturation and synaptic connection in the recipient brain. Even though further study is necessary to elucidate molecular and cellular mechanisms responsible for the functional recovery, we consider that the ES cells may have advantage for use as a donor source in various neurological disorders including motor dysfunction.
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http://dx.doi.org/10.1016/j.jns.2004.01.006 | DOI Listing |
Methods Mol Biol
December 2024
Department of Experimental Medicine, Biotechnology, and Molecular Biology Section, Luigi Vanvitelli Campania University, Naples, Italy.
Mesenchymal stromal cells (MSCs) are a heterogeneous population of non-hematopoietic adult stem cells derived from the embryonic mesoderm. They possess self-renewal and multipotent differentiation capabilities, allowing them to give rise to mesodermal cell types, such as osteoblasts, chondroblasts, and adipocytes, as well as non-mesodermal cells, including neuron-like cells and endothelial cells. MSCs play a vital role in maintaining homeostasis across various tissues by facilitating tissue repair, immune regulation, and inflammatory response balance.
View Article and Find Full Text PDFFront Cell Dev Biol
December 2024
Department of Ophthalmology, Tufts Medical Center, Tufts University School of Medicine, Boston, MA, United States.
The cornea is densely innervated to maintain the integrity of the ocular surface, facilitating functions such as sensation and tear production. Following damage, alterations in the corneal microenvironment can profoundly affect its innervation, potentially impairing healing and sensory perception. One protein frequently upregulated at the ocular surface following tissue damage is galectin-3, but its contribution to corneal nerve regeneration remains unclear.
View Article and Find Full Text PDFActa Neuropathol Commun
December 2024
Department of Physiology & Biophysics, Case Western Reserve University School of Medicine, Cleveland, OH, 44106, USA.
Mitochondrial dysfunction and α-synuclein (αSyn) aggregation are key contributors to Parkinson's Disease (PD). While genetic and environmental risk factors, including mutations in mitochondrial-associated genes, are implicated in PD, the precise mechanisms linking mitochondrial defects to αSyn pathology remain incompletely understood, hindering the development of effective therapeutic interventions. Here, we identify the loss of branched chain ketoacid dehydrogenase kinase (BCKDK) as a mitochondrial risk factor that exacerbates αSyn pathology by disrupting Complex I function.
View Article and Find Full Text PDFJ Cell Mol Med
December 2024
Laboratório de Produtos Naturais, Universidade São Francisco, Bragança Paulista, Brazil.
Alzheimer's disease (AD) is a progressive neurodegenerative disorder involving mitochondrial dysfunction and consequent production of reactive oxygen species (ROS), generated after amyloid peptide (Aβ42) accumulation. In this study, we isolated a new antioxidant molecule from the sun coral Tubastraea tagusensis and analysed it in cells exposed to oligomeric amyloid-beta peptide 1-42 (oAβ42). The coral was collected and immersed in methanol for the release of compounds, which were submitted to antioxidant DPPH and FRAP activity-guided fractionation using solid-phase extraction and HPLC.
View Article and Find Full Text PDFBiochem Biophys Res Commun
January 2025
Laboratory of Medical Therapeutics and Molecular Therapeutics, Japan. Electronic address:
A GGGGCC hexanucleotide repeat expansion (HRE) within the C9orf72 gene is a major causative factor in amyotrophic lateral sclerosis (ALS). This aberrant HRE results in the generation of five distinct dipeptide repeat proteins (DPRs). Among the DPRs, poly-PR accumulates in the nucleus and exhibits particularly strong toxicity to motor and cortical neurons.
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