MicroRNA and mRNA profiling of T cells from Acquired Aplastic Anaemia (AA) patients using both in-silico and in-vitro methods identified molecular changes, including altered immune-regulatory gene expression, linked to T-cell dysregulation and AA pathobiology. MicroRNA (GSE82095) and mRNA (GSE3807) profiles of T cells were obtained from patients with aplastic anaemia and controls using the GEO database. Differential expression was analyzed using GEO2R and TAC 4.0, selecting miRNAs and mRNAs with fold change >2 and an adjusted p-value <0.05. Enrichment analysis of significant miRNAs was conducted via miEAA2.0, while their gene targets were predicted using miRNet and validated with MiRTarBase, TargetScan, miRanda, and MiRDB. Functional enrichment of these targets was assessed using GSEA (FDR < 0.25). This workflow enabled a thorough evaluation of miRNA-mRNA interactions in AA. The T-cell dataset identified 41 miRNAs and 944 mRNA targets that were significantly altered in Aplastic Anemia (AA) cases versus controls (P<0.05). Venn diagram analysis showed all 944 differentially expressed genes overlapped with the 8305 possible mRNA targets of T-cell miRNAs, which were then used for GSEA to identify enriched gene ontology and pathways. Twenty top mRNA targets underwent further PPI network and hub gene analysis, highlighting 10 key pathways, including Interleukin-13, PI3K-Akt, IFN gamma, MAPK, hematopoietic lineage, mTOR, Interleukin- 4/13, TGF-beta, haemostasis, and cytokine receptor interaction. Network analysis identified 10 hub genes (e.g., EP300, CREBBP, CEBPB, CEBPA, FOS, NCOA3, ESR1, RUNX1, PPARG, and NCOR1) and common transcription factors (e.g., EP300, CREBBP, CEBPB, RUNX1, etc.). GSEA and DAVID analyses indicate these genes and pathways are closely involved in the immune pathogenesis of acquired AA. This study of miRNA and mRNA expression in T cells from acquired aplastic anemia patients shows significant molecular changes linked to immune dysregulation. Key miRNAs, hub genes, and pathways like IL-13, PI3K-Akt, and NOTCH may play a role in AA pathobiology. Analysis of protein interactions and transcription factors identified further regulatory nodes involved in abnormal immune responses. These findings reveal miRNA-mRNA networks in acquired aplastic anaemia and propose them as potential biomarkers or therapeutic targets, pending further experimental validation of their clinical significance. Computational analysis shows that miRNAs regulate key T-cell mRNA and signalling pathways in AA patients. Following experimental validation, these microRNA-target interactions could be explored for potential diagnostic or therapeutic roles in AA.

Bronchopulmonary dysplasia (BPD), a prevalent chronic pulmonary disorder predominantly affecting preterm infants, is characterized by impaired lung development and persistent inflammatory-mediated lung injury. Dermal fibroblast-derived exosomes (DF-Exos) have been demonstrated to alleviate inflammation and promote epithelial tissue repair; however, their role in lung injury remains to be elucidated. This study aimed to evaluate the effects of DF-Exos on BPD and explore their relationship with autophagy. DF-Exos were isolated using the ultracentrifugation method. Neonatal Sprague-Dawley (SD) rats were exposed to hyperoxic conditions (90% O₂) for 7 days to establish a BPD model. Lung morphology, pulmonary vasculature, and the expression of inflammatory mediators were assessed. The expressions of autophagy-related proteins Beclin1, LC3B, and p62 were detected to evaluate autophagy. Neonatal rats exposed to hyperoxic conditions showed alveolar simplification, reduced microvascular density, and a significant upregulation of pro-inflammatory mediators, including IL-1β, IL-6, and TNF-α. In contrast, the levels of the anti-inflammatory cytokine IL-10 showed no statistically significant alteration. The expression of autophagy-related protein Beclin1 and LC3B conversion decreased, and p62 accumulated. DF-Exos administration improved alveolar development, increased microvascular density, alleviated inflammation, facilitated the expression of Beclin1 and the conversion of LC3B, and reduced the expression of p62. Our study showed that in the BPD model, DF-Exos can promote alveolar repair and vascular regeneration, modulate inflammatory responses, and enhance autophagic activity. However, they may also cause transient lung injury in the early stages of development. This effect may be influenced by mild immune rejection. Further studies are needed to elucidate the underlying mechanisms and determine a safe therapeutic dose. DF-Exos partly ameliorated lung injury in the hyperoxia-induced BPD model, prospectively by enhancing autophagy.

The transmembrane protein TMEM175, a cation channel located on the lysosomal membrane, plays a crucial role in regulating lysosomal membrane potential and maintaining intralysosomal pH stability. It is involved in various physiological and pathological processes. This review summarizes recent advancements in understanding TMEM175's role in lysosomal physiology, with a detailed discussion of its regulatory mechanisms and specific contributions to lysosomal function. Furthermore, it explores the potential links between TMEM175 and human diseases, particularly neurodegenerative disorders. The structure of TMEM175 is elaborated upon, highlighting how activators and inhibitors interact with different structural domains of TMEM175, revealing multiple potential active sites. The functional significance of these sites and their relationships with TMEM175's activity are also discussed.

Stem cell-based therapy has emerged as a promising avenue for treating pulmonary degenerative disorders due to its remarkable capacity for self-renewal and differentiation into various cell types. However, concerns regarding undesired differentiation and tumorigenicity have raised questions about the safety and efficacy of cell-based therapy. The aim of the present systematic review study was to determine the therapeutic effectiveness of stem cell secretome in mitigating three pulmonary degenerative diseases, including Acute Lung Injury (ALI), Idiopathic Pulmonary Fibrosis (IPF), and Bronchopulmonary Dysplasia (BPD). A comprehensive search was carried out on international databases, including MEDLINE, Scopus, Web of Science, PubMed, and Embase, using related keywords according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA-2020) guidelines. Of 1541 retrieved studies, 136 articles were included in the present systematic review. The therapeutic effects of stem cells are primarily attributed to their paracrine secretions, specifically bioactive molecules known as the secretome, which includes exosomes and extracellular vesicles. Secretome-based therapy shows great promise in maximizing the healing potential of stem cells. However, several challenges and limitations hinder its widespread application, including scalability issues, delivery challenges, difficulty in controlling dosage, and the lack of standardized production protocols. As it is a novel therapeutic approach, its complex composition, mechanism of action, and variability in responses from the body, as well as long-term safety, remain unknown and pose challenges that necessitate further investigation and well-designed clinical trials. The secretome exerts its protective and therapeutic effects by regulating various processes, including inflammation, oxidative stress, cell apoptosis, macrophage polarization, growth factor signaling pathways, immune cell activation, TGF-β signaling pathways, angiogenesis, structural attenuation, fibrosis resolution, pulmonary functional improvement, and alveolarization.

We regret to inform you that the article titled "Expression and Function of PPARs in Cancer Stem Cells," published in Current Stem Cell Research & Therapy, Volume 11, Issue 3, 2016, is being retracted due to concerns regarding image manipulation and the reuse of images from unrelated studies by different authors, which depict findings from separate experiments. For example, Fig. (2) in the article appears to be identical to an image published in a study by Peters, J. et al. (2012), Nature Reviews Cancer, 12, 181-195 (https://doi.org/10.1038/nrc3214). When contacted for clarification, the authors were unable to provide the original/raw data to verify the authenticity of their results. In light of the lack of supporting evidence and the confirmed image duplication, the Editors have concluded that the findings of the article can no longer be considered reliable and have therefore recommended the retraction of the paper. We apologize for any inconvenience this may have caused and appreciate your understanding in this matter. Bentham Science Disclaimer: It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure, or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication, the authors agree that the publishers have the legal right to take appropriate action against the authors if plagiarism or fabricated information is discovered. By submitting a manuscript, the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication.

Mesenchymal Stem Cells (MSCs) are multipotent stem cells that are obtained from various tissue sources such as bone marrow, adipose tissues, umbilical cords, dental pulps, and peripheral blood has high regenerative potential, migratory abilities, and immunosuppressive properties. These properties make them attractive candidates for tissue engineering, immunosuppressive therapies, and in vivo drug deliveries. MSCs, because of their high propensity to home in an injured tissue microenvironment, are exposed to various cytokines. These cytokines modulate the activity of MSCs to help in the regeneration of injured tissue. Interleukins are one such cytokine that is present in injured tissue microenvironment and plays significant roles in the activation, differentiation, proliferation, maturation, migration, and adhesion of not only immune cells but also MSCs. Interleukins, through both autocrine and paracrine signaling mechanisms, modulate the functioning of MSCs. This article reviews how interleukins influence MSCs by discussing their signaling pathways, their effect on differentiation and other biological effects. A comprehensive understanding of the influence of interleukins on MSCs may provide insights to manipulate improving the therapeutic potential of MSCs or reducing potential risks such as undesirable immune response and tumor formation.

This study investigates the therapeutic potential of adipose-derived stem cells (ASCs) in diabetic foot ulcers (DFUs). The goal is to further research regenerative medicine by improving knowledge of ASC-based therapies in diabetic wound management. A comprehensive literature review included studies from reputable databases, including PubMed and the Cochrane Library. We paid particular attention to the clinical, in vivo, and in vitro investigations of the utility and effectiveness of ASCs in treating DFU. We also highlighted novel isolation techniques and application methods for ASCs in chronic wound management. ASCs have shown great potential in regenerative interventions for diabetes, especially in DFU management. These cells facilitate wound repair by differentiating into different cell types, promoting angiogenesis, secreting growth factors, reducing inflammation, and increasing wound perfusion. However, the current body of research on ASC applications for DFU still requires further investigation. This shows the importance of thoroughly studying their biological mechanisms and therapeutic uses. This review establishes that ASC-based treatments effectively enhance outcomes for patients suffering from DFU. We recommend further investigation of the functionality of ASCs and therapeutic approaches to maximize their therapeutic potential in managing diabetic wounds, thereby advancing the development of regenerative medicine.

Mesenchymal stem cells (MSCs) were able to restore ovarian function in premature ovarian insufficiency (POI), which can be largely attributed to the paracrine effects of MSCs therapy. However, the function and mechanism of MSC-derived exosomes transplantation for POI are not fully understood. To investigate the efficacy and underlying mechanisms of human placental derived MSCs derived exosomes (hpMSC-Exos) xenotransplantation in incremental load training-induced POI. The incremental exercise treadmill training was employed for constructing the POI rat model. hpMSC-Exos were administered to POI rats by tail vein injection. The ovarian function was assessed based on histological analysis and hormone levels. Ovarian function parameters, follicle counts, oocyte aging, granulosa cell apoptosis, and follicular microenvironment were evaluated. The tracking of hpMSC-Exos indicated that they generally colonized the ovarian tissues. hpMSC-Exos transplantation increased telomere length and telomerase activity, reduced oxidative stress, downregulated the Bax and caspase-3 gene expression, upregulated the Bcl-2 gene expression, and increased the insulin-like growth factor 1 (Igf-1) and vascular endothelial growth factor (VEGF) expression level. Furthermore, the findings showed that the follicle-stimulating hormone (FSH) level and FSH to luteinizing hormone (LH) ratio were decreased, whereas the population of follicles significantly increased after transplantation. hpMSC-Exos transplantation was observed to improve the function of the injured ovarian tissues in the incremental load training-induced POI rats. Furthermore, the mechanisms of hpMSC-Exos are related to delaying aging in the oocyte, reducing apoptosis of granulosa cells, and regulating the follicular microenvironment.

Human umbilical cord mesenchymal stem cell-derived exosomes (hucMSC-Exs) have been found to exhibit therapeutic effects on inflammatory bowel disease (IBD). However, due to the harsh environment of the gastrointestinal tract, exosomes, as a type of biological drug or carrier of bio-active substances, are still delivered by tail vein injection. In this study, hucMSC-Ex were coated with poly (lactic-co-glycolic acid) (PLGA) polymer to form microparticles, PLGA-hucMSC-Ex, by double emulsion method. The oral administration of PLGA-hucMSC-Ex particles alleviated inflammation in the mice model of IBD by reversing IBD-induced epithelial-mesenchymal transition (EMT). This provides an alternative to exploring IBD treatments, with potential clinical application to relieve IBD in patients.

Tissue homeostasis and regeneration depend on differentiated stem cells into specialized cell types. Dietary interventions, such as caloric restriction, are critical regulators of stem cell functions by altering their metabolism. This review discusses recent studies illustrating how diet interventions impact stem cell function. We summarize molecular targets and physiological effects of different types of caloric restriction and ketogenic mimicking diets in stem cells from bone marrow, muscle, and intestine. Furthermore, we highlight the nutrient-sensing pathway target of stem cells during caloric restriction. Understanding how nutrient signaling controls stem cell fate decisions is important to developing dietary interventions to improve the clinical application of stem cells.