Amniotic fluid-derived mesenchymal stem cells as a therapeutic tool against cytokine storm: a comparison with umbilical cord counterpartsVaiasicca, James, Melone
et alStem Cell Res Ther (2025) 16 (1), 151
Abstract: Several immunosuppressive therapies have been proposed as key treatment options for critically ill patients since the first appearance of severe acute respiratory syndrome coronavirus 2. Mesenchymal stem cells (MSCs) from different sources have been considered for their potential to attenuate the cytokine storm associated to COVID-19 and the consequent multi-organ failure, providing evidence for safe and efficacious treatments. Among them, administration of umbilical cord-derived MSCs (UC-MSCs) has demonstrated a significant increase in survival rates, largely due to their potent immunosuppressive properties.We applied next-generation sequencing (NGS) analysis to compare the transcriptomic profiles of MSCs isolated from two gestational sources: amniotic fluid (AF) obtained during prenatal diagnosis and their clinically relevant umbilical cord counterparts, for which datasets were publicly available. A full meta-analysis was performed to identify suitable GEO and NGS datasets for comparison between AF- and UC-MSC samples.Transcriptome analysis revelaed significant differences between groups, despite both cell lines being strongly involved in the tissue development, crucial to achieve the complex task of wound healing. Significantly enriched hallmark genes suggest AF-MSC superior immunomodulatory features against signaling pathways actively involved in the cytokine storm (i.e., IL-2/STAT, TNF-a/NFkB, IL-2/STAT5, PI3K/AKT/mTOR).The data presented here suggest that AF-MSCs hold significant promise for treating not only COVID-19-associated cytokine storms but also a variety of other inflammatory syndromes (i.e., those induced by bacterial infections, autoimmune disorders, and therapeutic interventions). Realizing the full potential of AF-MSCs as a comprehensive therapeutic approach in inflammatory disease management will require more extensive clinical trials and in-depth mechanistic studies.© 2025. The Author(s).
Tanshinone IIA + Osthole alleviates ferroptosis in LPS-induced acute lung injury by Keap1-Nrf2/HO-1 pathwayLi, Pan, Zhao
et alMicrob Pathog (2025)
Abstract: Acute lung injury (ALI) is associated with a high mortality rate and requires effective treatment. Tanshinone IIA (T) and Osthole (O) exhibit anti-inflammatory effects and have been used to protect against lipopolysaccharide (LPS)-induced lung injury in mice. However, the combined effects of T and O on lung injury protection and their potential protective mechanisms have not been studied.To assess the protective effects of TO on LPS-induced ALI in mice and BEAS-2B cell injury and to investigate the potential mechanisms underlying these protective effects.Models of ALI induced by LPS were established. The assessment encompassed the viability of BEAS-2B cells, cell count, myeloperoxidase (MPO) activity, protein content, as well as IL-6 and TNF-a levels in bronchoalveolar lavage fluid (BALF). Additionally, malondialdehyde (MDA), reactive oxygen species (ROS), and glutathione (GSH) levels in mouse lung tissue were measured. The effects of TO were assessed using immunofluorescence (IF), immunohistochemistry (IHC), Western Blot (WB), RT-PCR, and ELISA. Statistical analysis involved one-way ANOVA and t-test.TO administration led to a significant reduction in lung edema (W/D), MDA, ROS, GSH, and superoxide dismutase (SOD) levels compared to the individual T or O groups, alleviating LPS-induced ALI. TO also significantly attenuated lung tissue damage, reduced inflammatory response, decreased Fe2+ and 4-HNE levels, and increased GPX4, SLC7A11, and Nrf2 gene expression in mice. Ultimately, TO alleviated ferroptosis in LPS-induced ALI by activating Nrf2 expression, and no markedly adverse reactions were observed.TO alleviates LPS-induced ALI and effectively treats against LPS-induced ALI.Copyright © 2025. Published by Elsevier Ltd.
Sevoflurane Mediates LINC00339/miR-671-5p/PSMB2 Axis to Improve Cardiomyocytes Against Hypoxia/Reoxygenation InjuryLi, Mou, Yuan
et alJ Biochem Mol Toxicol (2025) 39 (4), e70234
Abstract: Ischemia/reperfusion (I/R) causes a deterioration in heart function, leading to myocardial infarction. It is aimed at investigating the protective mechanism of sevoflurane (Sevo) on cardiomyocytes by constructing a cellular model of hypoxic/reoxygenation (H/R) in this study.[Human hybrid] epithelioid cells (AC16) were induced by H/R to establish a model of myocardial I/R injury and Sevo postconditioning. The expression of long intergenic non-protein coding RNA 339 (LINC00339), microRNA-671-5p (miR-671-5p) and proteasome 20S subunit beta 2 (PSMB2) was detected by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Viability and apoptosis of AC16 cells were detected by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. The levels of interleukin-6 (IL-6), IL-10, tumor necrosis factor-a (TNF-a), reactive oxygen species (ROS), malondialdehyde (MDA), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD), were detected. LINC00339 expression was upregulated in H/R cardiomyocytes relative to the Control group, whereas Sevo decreased LINC00339 expression in H/R cardiomyocytes. The viability of AC16 cells were increased, and apoptosis, oxidative stress, and inflammatory responses decreased in the Sevo postconditioning group relative to the H/R group, but the protective effect of Sevo on H/R cardiomyocytes was partially reversed by LINC00339 overexpression. LINC00339 negatively regulated miR-671-5p, and miR-671-5p upregulation could alleviate the damage of LINC00339 on H/R cardiomyocytes. PSMB2, a downstream target gene of miR-671-5p, could inhibit the protective effect of Sevo on H/R cardiomyocytes. Sevo postconditioning exerts a protective effect in H/R-induced cardiomyocyte injury, which may be achieved by interfering with LINC00339/miR-671-5p/PSMB2 expression.© 2025 Wiley Periodicals LLC.
Aptamer-Based Graphene Field-Effect Transistor Biosensor for Cytokine Detection in Undiluted Physiological Media for Cervical Carcinoma DiagnosisWang, Dai, Zhang
et alBiosensors (Basel) (2025) 15 (3)
Abstract: Personalized monitoring of disease biomarkers is of great interest in women's health. However, existing approaches typically involve invasive inspection or bulky equipment, making them challenging to implement at home. Hence, we present a general strategy for label-free and specific detection of disease biomarkers in physiological media using an aptamer-based biosensor. The biosensor is a graphene field-effect transistor that involves immobilizing the aptamer and a biomolecule-permeable polyethylene glycol (PEG) layer on the graphene surface. The aptamer is capable of specifically binding with the target biomarker, thus inducing a change in the sensing responses. The PEG layer can effectively reduce the nonspecific adsorption of nontarget molecules in the solution, and increase the effective Debye screening length in the region directly adjacent to the graphene. In this work, studies of a biosensor with modification of the aptamer and PEG show that cervical carcinoma biomarkers such as tumor necrosis factor-α and interleukin 6 can be sensitively and specifically detected in undiluted physiological media, with detection limits as low as 0.13 pM for TNF-a and 0.20 pM for IL-6. This work presents a significant method for the general application of the biosensor for disease diagnosis in women's health.
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