Introduction: Patient-derived induced pluripotent stem cells (iPSCs) have been widely used as disease models to test new therapeutic strategies. Moreover, the regenerative potential of stem cells can be improved with the use of biologically active compounds. Our study was designed to explore the effect of honokiol, a small polyphenol molecule extracted from , on the survival and culture time of iPSC-derived neurons from a sporadic Alzheimer's disease (AD) patient. This study aimed to generate iPSCs from peripheral blood mononuclear cells (PBMCs) of an AD patient using episomal plasmids with a nucleofector system and differentiate them into neurons. These iPSC-derived neurons were used to investigate the effect of honokiol extracted from on their survival and long-term cultures.
Methods: IPSCs were generated from PBMCs of an AD patient by introducing Oct-3/4, Sox2, Klf4, L-Myc, and Lin28 using Nucleofector Technology. Differentiation of neurons derived from iPSCs was carried out using inducers and recognized by biomarkers. The viability of iPSC-derived neurons with the addition of honokiol extracted from the bark of was determined by the MTT analytical kit.
Results: IPSCs were generated by reprogramming AD patient-derived PBMCs and subsequently converted into neurons. The survival and growth of iPSC-derived neurons were significantly enhanced by adding honokiol in the experiment conditions.
Conclusion: AD iPSC-derived neurons had a high viability rate when cultured in the presence of honokiol. These results have shown that AD iPSC-derived neurons can be an excellent model for screening neurotrophic agents and improving the conditions for long-term cultures of human iPSC-derived neurons. Honokiol proves to be a potential candidate for cellular therapeutics against neurodegenerative disorders.
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http://dx.doi.org/10.34172/bi.2023.27652 | DOI Listing |
CNS Neurosci Ther
January 2025
Children's Medical Center, Department of Pediatric Neurology, Peking University First Hospital, Beijing, China.
Aims: Alexander disease (AxD) is a leukodystrophy caused by mutations in the astrocytic filament gene GFAP. There are currently no effective treatments for AxD. Previous studies have rarely established AxD models with the patient's original GFAP mutations.
View Article and Find Full Text PDFCell Death Discov
January 2025
Bioinnovation Center, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.
The neuromuscular junction (NMJ) is essential for transmitting signals from motor neurons (MNs) to skeletal muscles (SKMs), and its dysfunction can lead to severe motor disorders. However, our understanding of the NMJ is limited by the absence of accurate human models. Although human induced pluripotent stem cell (iPSC)-derived models have advanced NMJ research, their application is constrained by challenges such as limited differentiation efficiency, lengthy generation times, and cryopreservation difficulties.
View Article and Find Full Text PDFGenes (Basel)
January 2025
Department of Ophthalmology, Boston Children's Hospital, Boston, MA 02115, USA.
Background/objectives: Strabismus is the most common ocular disorder of childhood. Three rare, recurrent genetic duplications have been associated with both esotropia and exotropia, but the mechanisms by which they contribute to strabismus are unknown. This work aims to investigate the mechanisms of the smallest of the three, a 23 kb duplication on chromosome 4 (hg38|4:25,554,985-25,578,843).
View Article and Find Full Text PDFMol Cell Proteomics
January 2025
Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048; Advanced Clinical Biosystems Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048; Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048. Electronic address:
Single cell proteomics was performed on human induced pluripotent stem cells (iPSCs), iPSC-derived cardiomyocytes, and adult cardiomyocytes. Over 700 proteins could be simultaneously measured in each cell revealing unique subpopulations. A sub-set of iPSCs expressed higher levels of Lin28a and Tra-1-60 towards the outer edge of cell colonies.
View Article and Find Full Text PDFHum Mol Genet
January 2025
Department of Human Genetics, Inselspital Bern, University of Bern, Freiburgstrasse 15, Bern 3010, Switzerland.
While de novo missense variants in the BTB domains of atypical RhoGTPase RHOBTB2 cause a severe developmental and epileptic encephalopathy, de novo missense variants in the GTPase domain or bi-allelic truncating variants are associated with more variable neurodevelopmental and seizure phenotypes. Apart from the observation of RHOBTB2 abundance resulting from BTB-domain variants and increased seizure susceptibility in Drosophila overexpressing RhoBTB, our knowledge on RHOBTB2-related pathomechanisms is limited. We now found enrichment for ion channels among the differentially expressed genes from RNA-Seq on fly heads overexpressing RhoBTB.
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