Acute Spinal Cord Injury (SCI) often causes motor and sensory deficits. SDF-1 promotes stem cell survival and proliferation, while FBN1 may impact repair mechanisms. This study investigates how SDF-1 promotes SCI treatment by inducing BMSC maturation through BMP-8-mediated FBN1 inhibition. Bone marrow mesenchymal stem cells were induced to differentiate with BMP-8 and transfected with related plasmids (oe-NC, oe-SDF-1, oe-FBN1, si-BMP-8). CCK-8 and alizarin red staining were used to assess cell growth and differentiation. Western blotting was used to detect the levels of SDF-1, FBN1, and BMP-8. In a rat SCI model, cells with plasmids were injected, and motor recovery was assessed using BBB scoring. Immunofluorescence assay detected SDF-1 expression, while Western blotting was used to detect SDF-1, FBN1, and BMP-8. In cell experiments, BMP-8 induced successful differentiation of BMSCs. After overexpression of SDF-1, the proliferation and differentiation of BMSCs were increased. In animal experiments, the BBB score increased after overexpression of SDF-1. These findings suggest a potential therapeutic mechanism in which SDF-1 promotes spinal cord repair by modulating the BMP-8/FBN1 axis. The suppression of FBN1 appears to be a key step in enhancing BMSC function. Targeting this pathway could offer new strategies for regenerative treatment following SCI. In acute spinal cord injury, SDF-1 enhances the differentiation of bone marrow mesenchymal stem cells induced by BMP-8 through the suppression of FBN1.

Acute myeloid leukemia (AML) arises from the aberrant proliferation of white blood cells, red blood cells, or platelets. Various therapy modalities are available for individuals diagnosed with AML. While Cytarabine remains a standard treatment, exosomes, especially those derived from cord blood, have emerged as promising adjuncts. Exosomes are a specific kind of extracellular vesicles that have been identified as candidate biomolecules for the treatment of AML. The current study looked at how cord blood-derived exosomes affect the U937 cell lines compared to Cytarabine as a fundamental component of standard AML treatment. The first stage involved processing umbilical cord blood and isolating the mononuclear cells, CB-MNCs. The exosomes were isolated and verified using transmission electron microscopy, western blotting, and dynamic light scattering. Subsequently, for 72 hours, the U937 cells were cultivated and exposed to the exosomes, Cytarabine, and a combination of both. Afterward, apoptosis was evaluated using flow cytometry. The activity of Caspase 3/7 was assessed using a special kit. The real-time PCR technique was used to evaluate the gene expression in the proliferation and apoptosis pathways. Finally, the activity of NF-κB and AMPK was assessed using western blotting. The flowcytometry analysis showed that the apoptosis rate of U937 cells after being exposed to CB-MNC exosomes, Cytarabine, and a mix of them was 19.60 (p < 0.05) %, 44.05 % (P < 0.0001), and 47.45 % (P < 0.0001), respectively. The activity of Caspase 3-7 was 0.32 mU/mL and 0.45 mU/mL (P < 0.001) Cytarabine and Mix groups. The qRT-PCR study revealed a notable upregulation of apoptotic genes and a downregulation of anti-apoptotic gene expression in the Mix group. Western blot analysis revealed a decrease in NF-κB phosphorylation in all treatment groups. In addition, the phosphorylation of AMPK increased in all treatment groups. The study evaluated the effects of CB-MNC-derived exosomes on U937 cells, both alone and in combination with Cytarabine. Results demonstrated that while exosomes induced moderate apoptosis, their combination with Cytarabine significantly enhanced cell death, increased Caspase 3/7 activity, and altered gene expression in favor of apoptosis. The treatment also inhibited NF-κB and activated AMPK signaling pathways. In conclusion, our findings indicated that CB-MNCs-derived exosomes together with Cytarabine have a cooperative effect on U937 cells through increasing apoptosis rate and reducing the proliferation rate, and may serve as a promising adjunct in AML therapy.

Diabetic foot ulcer (DFU) is a severe complication of diabetes mellitus, affecting up to 15% of diabetic patients and leading to high rates of hospitalization, morbidity, and lower limb amputation. This case study details the management of a 67-year-old diabetic male patient with a DFU complicated by osteomyelitis. The patient, with a long history of diabetes and multiple comorbidities, was treated with a comprehensive regimen that included antibiotics, debridement, and platelet-rich plasma (PRP) therapy. PRP was administered weekly for 15 weeks. Clinical, laboratory, and imaging data were employed for the evaluation of the disease improvement. As a result, a marked improvement in wound healing was observed, characterized by reduced wound size, accelerated closure of the wound, and enhanced tissue regeneration. However, the patient developed deep vein thrombosis, which was successfully managed with anticoagulants. The study highlights PRP's potential in DFU treatment due to its regenerative properties despite the risk of adverse effects. The efficacy of PRP aligns with previous studies, showing improved healing rates and infection control. Future research should focus on large-scale trials to optimize PRP protocols and confirm the safety and efficacy of this therapeutic method in DFU.

This study aims to explore the therapeutic potential of mesenchymal stem cells (MSC) in treating diabetic nephropathy (DN) by investigating their effect on IL-11 modulation in a mouse model. The effects of MSC therapy on DN were examined both in vivo and in vitro. Sixty adult male C57BL/6 mice were divided into the streptozotocin (STZ) diabetes (T1D) and the high-fat diet diabetes (T2D) models, with both groups receiving MSC treatment or saline for 4 or 8 weeks. Blood glucose, serum urea, interleukin-11 (IL-11), and kidney fibrosis markers were measured. Additionally, western blotting was used to assess levels of Type I and III collagen, E-Cadherin, α- smooth muscle actin (α-SMA), Vimentin, and ferroptosis suppressor protein 1 (FSP-1). MSC-treated T1D and T2D mice showed reduced blood glucose, serum urea, IL-11, TGF-β, and fibrosis markers (type I and III collagen, α-SMA, Vimentin, FSP-1), alongside increased E-Cadherin expression. Similar effects were observed in vitro using mouse glomerular epithelial cells, confirming MSC-mediated suppression of fibrosis pathways. MSC therapy improves nephropathy, likely by inhibiting IL-11 and reducing fibrosis- related markers, making it a promising treatment for DN.

Hematopoietic stem cells (HSCs) represent the most primitive cell population endowed with the ability for self-renewal and differentiation. They possess the capacity to differentiate into all types of blood cells, each serving unique functions. Traditional theories have established a clear hierarchical relationship between HSCs, their progenitors, and mature blood cells. The identification of distinct cell populations within the hematopoietic system forms the foundation of the hematopoietic differentiation model. However, recent research has led to a constant evolution of our understanding of the hierarchical structure of hematopoietic differentiation, particularly in the context of megakaryocyte differentiation pathways. Megakaryocytes are essential for platelet production, a critical process in hemostasis and thrombosis. Understanding the mechanisms underlying megakaryocyte-biased HSCs differentiation holds significance for both basic research and clinical applications. In this review, we consolidate the latest research progress concerning the evidence supporting these nonclassical pathways of megakaryocytic differentiation. Furthermore, we delve into the alterations observed in these pathways under conditions of steady state, transplantation, stress, and aging.

Fetal Bovine Serum (FBS), the conventional supplement for Mesenchymal Stromal Cell (MSC) culture, presents ethical issues, batch variability, and risks of pathogen transmission. This study aimed to evaluate human-derived Umbilical Cord Serum (UCS) and Human Platelet Lysate (HPL) as xeno-free alternatives to FBS and to assess the synergistic effects of nano-curcumin and crocin as supplements to enhance the proliferation and survival of human umbilical cord-derived MSCs. Human umbilical cord-derived MSCs were cultured in media supplemented with 10% FBS (control), UCS, or HPL. These groups were further treated with nano-curcumin (0.3 μM) or crocin (2.5 μM), either individually or in combination. Cell proliferation was measured using the MTT assay, apoptosis was assessed by Annexin V/PI flow cytometry, and pluripotency gene expression (Sox2, Nanog, Oct4) was analyzed by RT-qPCR. UCS and HPL supplements significantly increased MSC proliferation compared to the FBS control (p < 0.001). Specifically, UCS reduced the population doubling time by approximately 50%. Supplementation with crocin reduced apoptosis by up to 30% (p = 0.04) and significantly enhanced the expression of the pluripotency genes Sox2 and Nanog, particularly in cultures supplemented with HPL. In contrast, nano-curcumin inhibited MSC proliferation and increased apoptosis across all tested conditions. The results demonstrate that UCS and HPL are effective, viable alternatives to FBS, promoting superior MSC expansion. The anti-apoptotic and stemness-enhancing properties of crocin highlight its potential as a valuable additive for improving culture quality and cell survival. The cytotoxic effects observed with nano-curcumin underscore a critical need for dose-optimization studies. The primary limitation of this study is the use of fixed concentrations for the supplements, which warrants further investigation across a range of doses. UCS and HPL are robust, ethically sound replacements for FBS in MSC biomanufacturing. Crocin can further enhance culture outcomes by improving cell survival and maintaining stem cell properties. These findings support the development of optimized, xeno-free culture systems for scalable MSC production, which is crucial for advancing regenerative medicine therapies.

Intra-articular injection of autologous microfragmented adipose-derived mesenchymal stem cells (AMSCs) has shown potential for symptom relief and cartilage regeneration in osteoarthritis (OA). However, histological evidence in humans remains limited. We present a 46-year-old female patient who had symptomatic left hip OA and underwent a single injection of autologous microfragmented AMSCs under ultrasound guidance after unsuccessful hip arthroscopy. At the 12-month follow-up, the patient was pain-free, fully mobile, and had returned to normal daily activities without limitations, indicating an excellent clinical outcome. Eighteen months after the treatment, due to symptom recurrence, the patient later underwent total hip arthroplasty, allowing histological analysis of the joint. Examination revealed areas of hyaline-like cartilage in regions previously affected by degeneration. This case provides clinical and histological evidence of cartilage regeneration following intra-articular autologous microfragmented AMSCs therapy for hip OA. Although symptom recurrence occurred at 18 months, findings suggest this treatment may offer a regenerative option warranting further study.

Exosomes produced by mesenchymal stem cells (MSCs) have lately garnered significant attention for their capacity to enhance wound healing. Recent studies have recognized exosomes as significant secretory products from several cell types, specifically MSCs, in regulating multiple biological processes, including wound healing. This work aims to investigate the impact of exosomes derived from the bone marrow mesenchymal stem cells (BMMSCs) of NMRI animals on keratinocyte function. Exosomes were extracted from BMMSCs using a flushing technique and afterwards cultivated. Stem cells were detected via flow cytometry, while exosomes were isolated and purified through ultracentrifugation. The exosomes were analyzed using various techniques, including scanning electron microscopy (SEM), atomic force microscopy (AFM), transmission electron microscopy (TEM), and dynamic light scattering (DLS). The MTT assay and trypan blue staining were employed to assess the effect of exosomes on keratinocyte viability. A scratch assay was performed to evaluate cell migration after treatment with exosomes. Real-time PCR was employed to evaluate the expression of genes such as KGF, MMP3, VEGF, and TGF-β3. Keratinocytes exposed to 10 μg/mL of exosomes exhibited markedly enhanced viability relative to the control group. The group treated with exosomes had more cell migration compared to the control group. The therapy group had elevated expression levels of the KGF, MMP3, VEGF, and TGF-β3 genes. The experimental findings indicate that exosomes derived from BMMSCs enhance keratinocyte viability, proliferation, migration, and gene expression. A comprehensive study of the factors affecting exosome generation, isolation, and mechanisms of action is crucial, as their potential use in wound healing facilitates the development of innovative and highly effective therapeutic strategies.

Idiopathic Nephrotic Syndrome (INS) is a common kidney disease in children, and the main clinical manifestations are hypoproteinaemia, proteinuria, hyperlipidaemia, and oedema. Mesenchymal Stem Cells (MSCs) are involved in tissue repair, protection against fibrosis, and immune modulation but have rarely been studied in INS. This study aimed to explore the therapeutic potential of stem cells derived from human exfoliated deciduous teeth (SHEDs) in INS using an adriamycin-induced nephropathy (AN) rat model. AN was induced in Sprague‒Dawley rats, and SHEDs were transplanted via the tail vein in single (SHED-s) and multidose (SHED-m) regimens. Cell migration assays were used to track the SHED distribution. Weight, urine protein, and serum biochemical assays were also performed. HE and Masson staining were used to observe glomerular and tubular damage, as well as the degree of fibrosis. Immunohistochemistry was used to label T lymphocytes and podocytes, and structural changes in podocytes were observed by electron microscopy. ELISA was used to measure the levels of inflammatory factors. Flow cytometry was used to analyse the balance of Th17 cells and Tregs. The mRNA expression of Th17- and Treg-associated cytokines and specific transcription factors was examined by RT‒PCR. SHEDs directly migrated to damaged tissues, suggesting a targeted therapeutic effect. SHED transplantation significantly reduced proteinuria and reversed biochemical abnormalities in rats with AN. Both single and multidose SHED treatments could inhibit glomerular and tubular damage and delay the progression of fibrosis caused by adriamycin. SHEDs exerted a protective effect on podocytes. Additionally, this treatment inhibited inflammatory responses and corrected immune imbalances, as evidenced by decreased T lymphocyte infiltration, reduced serum levels of IL-6, TNF-a, and IL-1β, and modulation of the Th17/Treg balance. In the AN rat model, SHED partly suppressed the development of inflammation and alleviated kidney injury, and immune regulation may be the underlying mechanism.

Human adipose-derived stem cells (hADSCs) are considered a promising source for cell replacement therapy in degenerative and traumatic conditions. This study explores the effects of phenylacetate and calcium on the neural differentiation of hADSCs for regenerative medicine. We assessed cell viability and cytotoxicity using the MTT assay, revealing that treatment with 1μM phenylacetate significantly enhanced cell viability compared to control groups over five days, while higher concentrations resulted in cytotoxic effects. Additionally, qualitative analysis through Acridine orange/ethidium bromide (AO/EB) staining indicated normal cellular characteristics at lower phenylacetate concentrations, whereas higher doses led to observable cell death. A subsequent evaluation of intracellular calcium levels demonstrated a significant increase when hADSCs were treated with both phenylacetate and calcium. The neural differentiation potential was further assessed through the relative quantification of neuronal-specific genes, showing marked upregulation of NSE, Oligo-2, β-tubulin III, and MAP-2 in all treatment groups compared to controls. Immunohistochemistry confirmed elevated protein expression of neural markers in cultures supplemented with phenylacetate and calcium. These findings suggest that phenylacetate, particularly in conjunction with calcium, enhances the neural differentiation of hADSCs, highlighting its potential utility in regenerative medicine strategies targeting neurodegenerative conditions.