Neuroinflammation is regarded as one of the pathogenic factors of Alzheimer disease (AD). Previously, we showed that mice regularly injected with bacterial lipopolysaccharide (LPS) possessed the AD-like symptoms like episodic memory decline, elevated amounts of amyloid beta (Aβ) peptide (1–42), and decreased levels of nicotinic acetylcholine receptors (nAChRs) in the brain. The use of mesenchymal stem cells (MSCs), which can differentiate into multiple cell types, including neurons, is an attractive idea of regenerative medicine, in particular, for neurodegenerative disorders like AD. In the present study, we aimed to investigate whether pathogenic effect of LPS on the brain and behavior of mice can be prevented or treated by injection of MSCs or MSC-produced soluble factors. Fluorescently-labeled MSCs, injected intravenously, were found in the brain blood vessels of LPS-treated mice. Mice co-injected with LPS and MSCs did not demonstrate episodic memory impairment, Aβ (1–42) accumulation, and nAChR decrease in the brain and brain mitochondria. Their mitochondria released less cytochrome c under the effect of Ca²⁺ compared to mitochondria of LPS-only-treated mice. Moreover, MSCs could reverse the pathogenic symptoms developed 3 weeks after LPS injection. Cultured MSCs produced IL-6 in response to LPS and MSCs effect in vivo was accompanied by additional stimulation of both micro- and macroglia. Xenogeneic (human) MSCs were almost as efficient as allogeneic (mouse) ones and regular injections of human MSC-conditioned medium also produced positive effect. These data allow suggesting MSCs as a potential therapeutic tool to cure neuroinflammation-related cognitive pathology.

The development of efficient, biocompatible scaffolds is an actual challenge in tissue engineering. Scaffolds derived from animal sources offer promising structural and biochemical properties but require thorough decellularization to minimize immunogenicity and maintain extracellular matrix integrity. Effective decellularization requires a synergistic combination of methods to ensure complete removal of immunogenic cellular components while preserving critical extracellular matrix elements such as glycosaminoglycans, collagens, and growth factors. This review covers the application of some decellularization methods (physical, chemical) in scaffold production, highlighting their respective advantages, limitations, and biosafety considerations. Moreover, the importance of scaffold sterilization: both physical techniques like gamma irradiation and chemical agents–are mentioned for their efficacy and cytotoxic risks. Furthermore, scaffold modifications, particularly recellularization strategies, are discussed as key enhancements to improve biocompatibility and functional integration. Overall, the selection and optimization of decellularization protocols are crucial for the safe and effective clinical implementation of bioengineered scaffolds.

The hippocampus is the most susceptible region of the brain to ischemic lesion, with highly vulnerable pyramidal interneurons to ischemic cell death. A restricted brain neurogenesis limits a withdrawal of massive cell death after stroke that endorses cell-based therapies for neuronal replacement strategies following cerebral ischemia. Neurons differentiated from neural stem/progenitor cells (NSPCs) matured and integrated into host circuitry, improving recovery after stroke. However, how host environment regulates the NSPC behaviour in post-ischemic tissue remains unknown. Here we studied functional maturation of NSPCs in control and post-ischemic hippocampal tissue after modelling cerebral ischemia in situ. We traced maturation of electrophysiological properties and integration of the NSPC-derived neurons into the host circuits, developing appropriate activity that takes 3 weeks or less after engraftment. In the ischemic-injured tissue, the NSPC-derived neurons exhibited functional deficits and differentiation of embryonic NSPCs was boosted to glial type – oligodendrocytes and astrocytes. Our findings of the delayed neuronal maturation whilst the promoted NSPC differentiation towards glial cell type in post-ischemic conditions provide new insights into stem-cell-therapy for replacement strategies in cerebral ischemia.

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We have investigated the characteristics of human hematopoietic progenitor cells (HPCs) with the CD34⁺CD45^lowSSC^lowphenotype from full-term placental tissue (FTPT) as compared to cord blood (CB) and fetal liver (FL) cells. We demonstrated the presence of cell subpopulations at various stages of the differentiation with such immunophenotypes as CD34^+/lowCD45low/-, CD34⁺⁺CD45low/-, CD34⁺⁺⁺CD45low/-,CD34+/lowCD45^hi, and CD34⁺⁺CD45^hiin both first trimester placental tissue (FiTPT) and FTPT which implies their higher phenotypic heterogeneity compared to CB. HPCs of the FTPT origin expressed the CD90 antigen at a higher level compared to its expression by the CB HPCs and the CD133 antigen expression being at the same level in both cases. The HPCs compartment of FTPT versus CB contained higher number of myeloid and erythroid committed cells but lower number of myeloid and lymphoid ones compared to FL HPCs. HPCs of the FTPT and CB origin possess similar potentials for the multilineage differentiationin vitroand similar ratios of myeloid and erythroid progenitors among the committed cells. This observation suggests that the active hematopoiesis occurs in the FTPT. We obtained viable HPCs from cryopreserved placental tissue fragments allowing us to develop procedures for banking and testing of placenta-derived HPCs for clinical use.