Organoids are rapidly self-organizing 3D in vitro cultures derived from pluripotent stem cells (PSCs) or adult stem cells (ASCs) that possess disease-like characteristics with high success rates. Due to their ability to retain tissue structure, biological phenotypes, and genetic information, they have been utilized as a novel in vitro model for disease research. In recent years, scientists have established self-organizing 3D organoids for human endometrium, fallopian tubes, ovaries, and cervix by culturing stem cells with cytokines in 3D scaffolds. The integration of organoids with animal models, organ-on-a-chip systems, and 3D printing technologies offers a novel preclinical model for exploring disease mechanisms and developing treatments. This review elaborate on the recent research progress of stem cells-formed organoids in the field of gynecology from the aspects of constructing gynecological disease organoids, drug screening and new drug development, simulation modeling, allogeneic transplantation, regenerative medicine and personalized treatment."
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http://dx.doi.org/10.1007/s12015-024-10833-0 | DOI Listing |
Immunology
December 2024
Department of Molecular and Medical Pharmacology, UCLA, Los Angeles, California, USA.
Autoreactive, aberrantly activated lymphocytes that target myelin antigens in the central nervous system (CNS) are primary drivers of the autoimmune disease multiple sclerosis (MS). Proliferating cells including activated lymphocytes require deoxyribonucleoside triphosphates (dNTPs) for DNA replication. dNTPs can be synthesised via the de novo pathway from precursors such as glucose and amino acids or the deoxyribonucleoside salvage pathway from extracellular deoxyribonucleosides.
View Article and Find Full Text PDFMol Neurobiol
December 2024
Department of neurology, The Third Affiliated Hospital, Sun Yat-sen University, 600 Tianhe Road, Guangzhou, 510630, Guangdong, China.
Aims: This study aims to elucidate the therapeutic effects and underlying mechanisms of exosomes derived from Heme oxygenase 1 (HO-1)-overexpressing human umbilical cord mesenchymal stem cells (Exo) in a subarachnoid hemorrhage (SAH) mouse model.
Methods: In this study, exosomes were identified using Western blotting, particle analysis, and transmission electron microscopy. The effect of Exo and Exo on the neurological function of SAH mice was assessed using the Garcia scoring system, Beam balance, Rotarod test, and Morris water maze test.
Skelet Muscle
December 2024
School of Biological Sciences, Seoul National University, Seoul, 08826, Republic of Korea.
Background: Muscle stem cells (MuSCs) undergo numerous state transitions throughout life, which are critical for supporting normal muscle growth and regeneration. Epigenetic modifications in skeletal muscle play a significant role in influencing the niche and cellular states of MuSCs. Mixed-lineage leukemia 4 (Mll4) is a histone methyltransferase critical for activating the transcription of various target genes and is highly expressed in skeletal muscle.
View Article and Find Full Text PDFDiabetol Metab Syndr
December 2024
Nervous System Stem Cells Research Center, Semnan University of Medical Sciences, Semnan, Iran.
Obesity is a multifactorial condition influenced by genetic, environmental, and microbiome-related factors. The gut microbiome plays a vital role in maintaining intestinal health, increasing mucus creation, helping the intestinal epithelium mend, and regulating short-chain fatty acid (SCFA) production. These tasks are vital for managing metabolism and maintaining energy balance.
View Article and Find Full Text PDFJ Biol Chem
December 2024
Department of Biological Sciences, University of Memphis, Memphis, TN 38152, USA. Electronic address:
Mitogen-activated protein kinase kinase kinase 4 (MAP3K4) promotes fetal and placental growth and development, with MAP3K4 kinase inactivation resulting in placental insufficiency and fetal growth restriction. MAP3K4 promotes key signaling pathways including JNK, p38, and PI3K/Akt, leading to activation of CREB-binding protein. MAP3K4 kinase inactivation results in loss of these pathways and gain of histone deacetylase 6 (HDAC6) expression and activity.
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