Current stem cell research & therapy最新文献

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.

End-stage liver disease (ESLD) poses a significant threat to human health due to its high mortality rate. Although liver transplantation represents the most effective treatment modality, its application is limited by donor scarcity and prohibitive costs, thereby necessitating the development of innovative and efficacious therapeutic strategies. Within the realm of regenerative medicine, stem cell therapy has emerged as a promising alternative for ESLD treatment, with mesenchymal stem cells (MSCs) being at the forefront due to their exceptional multifunctional differentiation and self-renewal capabilities. Nonetheless, safety concerns, including the potential risk of tumorigenesis associated with MSCs, remain inadequately addressed. Recent evidence indicates that the therapeutic effects of MSCs are primarily mediated through paracrine mechanisms, with MSC-derived exosomes (MSC-Exos) serving as the principal effector mediators. The utilization of exosomes alone for therapeutic purposes not only preserves the beneficial effects of MSCs but also mitigates risks such as tumorigenic potential. Over the past few years, MSC-Exos have demonstrated significant ad-vancements across various medical disciplines, including cardiology, neurology, and gastroenterology. This review outlines the key mechanisms and recent progress in utilizing MSC-Exos in treating end-stage liver disease, seeking to highlight their unique therapeu- tic role.

Background: Stem cells have recently gained prominence in regenerative medicine, particularly in the treatment of neurological disorders. As a result, Human-induced Pluripotent Stem Cells (hiPSCs) have become a significant focus.

Objective: This study aimed to differentiate hiPSCs into neural lineages under in vitro conditions using forskolin and retinoic acid in an induction medium combined with chondroitin 4-sulfate and chondroitinase.

Methods: Optimal component concentrations were determined using the MTT assay and acridine orange/ethidium bromide (AO/EB) staining. Subsequently, neural-specific genes (NSE, MAP-2, β-tubulin III, Oligo-2, and GFAP) and proteins (gamma enolase, MAP-2, and β-tubulin III) were assessed using Real-time PCR analysis and immunofluorescence staining to provide a comprehensive evaluation of differentiated cells.

Results: Our study demonstrated a significant enhancement in neural-specific gene and protein markers during the 7th and 14th days of differentiation in the presence of combined chondroitin 4-sulfate and chondroitinase, demonstrating a higher efficacy compared with the application of isolated enzymes or substrates.

Conclusion: These findings emphasize the potential importance of chondroitin 4-sulfate and chondroitinase as important factors in promoting the neural differentiation of hiPSCs. It seems that chondroitin 4-sulfate may activate cellular signaling pathways that are effective in inducing neural differentiation. Our findings in this research provide new opportunities to advance regenerative therapies for neurological disorders.

Cancer is a predominant cause of mortality globally, with both incidence and mortality rates consistently rising. The integrative nature of cancer, characterised by the coexistence of malignant and normal cells, diminishes the efficacy of single-modality therapies for both early-stage and late-stage tumours. Consequently, multimodal interventions, including surgery, radiation, chemotherapy, and immunotherapy, are necessary. Patient heterogeneity and cancer resistance complicate treatment outcomes, requiring personalised therapeutic approaches. Cancer cells operate as astute entities, collaborating with the human body to circumvent treatment, thus necessitating correspondingly intricate therapeutic approaches. Existing medicines are insufficient, rendering cancer a continual struggle for medical professionals and researchers. The progression of nanotechnology has led to the emergence of theranostics, which combines diagnosis and therapy into a unified approach. Nanotheranostic drugs, influenced by external stimuli such as light, magnetic fields, and ultrasound, signify a novel advancement in anti-cancer treatments. Although numerous stimuli-responsive theranostic nanomaterials have demonstrated proof-of-concept, none have progressed to clinical trials. This chapter examines diverse theranostic nanomaterials, emphasising inorganic agents utilised without chemical alterations. It evaluates the efficacy of theranostic agents licensed for preclinical and clinical trials. Chemotheranostics, radiotheranostics, immunotheranostics, and phototheranostics present considerable potential owing to their extensive surface area, customisable attributes, and biocompatibility. Notwithstanding significant progress, difficulties, including particle size, charge, medication stability, and surface changes, remain. Interdisciplinary collaboration among biological, pharmaceutical, materials science, and nanotechnology sectors is crucial for enhancing clinical translation. Tumor-specific theranostic biomaterials offer a targeted methodology, minimising toxicity and improving therapeutic efficacy while accounting for individual patient chracteristics.

Background: Parkinson's disease (PD) is a chronic progressive neurodegenerative disease with debilitating clinical presentations. Common therapeutic approaches for symptomatic improvement are often effective for a temporary period of time, after which patients often experience progressive disabilities. Cell replacement therapy is a potential therapeutic method that aims to replace depleted mesencephalic dopaminergic (DA) neurons, which may control symptoms and halt disease progression. Preclinical studies have investigated the efficacy of these PSC-derived DA cells in animal models of PD.

Methods: In this study, we comprehensively examine preclinical data on the therapeutic effect of primate PSC-derived DA progenitors on motor deficits in animal models of PD as a precursor for conducting human clinical trials. Relevant articles published before August 14th, 2023, were obtained from PubMed, Scopus, and Web of Science.

Results: Through several rounds of screening, 46 studies that met our inclusion criteria were included in this study. The quality of each study was assessed using CAMARADES and SYRCLE approaches. Although no included studies were judged to have an overall high risk of bias, several studies exhibited domain-specific methodological limitations. The analyzed studies demonstrate that cell therapy significantly improves motor dysfunction in rodent and non-human primate models of PD.

Conclusion: This systematic review and meta-analysis demonstrate that PSC-based cell therapy significantly improves motor dysfunction in rodent and NHP models of PD and could be a promising approach for halting disease progression, improving behavioral manifestations of the disease, and increasing the overall quality of life in PD.

Endometriosis is a chronic condition where tissue similar to the endometrium grows outside the uterus, affecting 5-10% of women and causing pelvic pain, painful periods, and infertility. Diseases of the endometrium, the lining of the uterus, can lead to a variety of reproductive health issues, including infertility, irregular bleeding, and endometrial cancer. Researchers have developed advanced in vitro systems using uterine organoids and decellularized tissue scaffolds to understand and model these diseases. The main limitations of traditional 2D monolayer cultures include reduced biological activity, reduced hormone responsiveness, and lack of interaction with ECM. Researchers have investigated 3D culture approaches to address these shortcomings, such as scaffold-free organoids and decellularized tissue scaffolds. Organoid systems can better recapitulate the cellular heterogeneity and physiological functions of the native endometrium. Decellularization protocols have been optimized to generate intact uterine scaffolds that preserve the structural and compositional features of the ECM. Implantation of these bioscaffolds into animal models demonstrated their biocompatibility and regenerative potential. Further refinements of organoid and scaffold technologies, including chemically defined matrices and organ-on-a-chip platforms, will improve our ability to model the uterus. Integration of these advanced in vitro models with patient-derived cells will enable personalized disease modeling and the development of targeted therapies. The combination of organoids, decellularized scaffolds, and microfluidic technologies holds great potential for exploring reproductive biology, drug screening, and developing regenerative therapies for uterine diseases and infertility.

Objectives: Epidermal growth factor-like domain-containing protein 6 (EGFL6) is a member of the epidermal growth factor superfamily. It has been reported that it can enhance the osteogenic differentiation potential of stem cells and stimulate angiogenesis. However, its effects on the regulation of odontogenic differentiation of dental pulp stem cells (DPSCs) have not been studied. Therefore, we aimed to investigate the role of EGFL6 in pulp regeneration and its underlying mechanism.

Methods: The cytotoxicity and migration-inductive ability of EGFL6 were evaluated using cell counting kit-8 assay and transwell assay, respectively. A tube formation assay was performed to assess the angiogenic effect of EGFL6. The alkaline phosphatase (ALP) and alizarin red S staining were conducted for mineralization evaluation. The odontoblastic-related and angiogenesis-related markers were measured by quantitative real-time polymerase chain reaction and Western blot analysis. Western blot was also conducted to further examine the levels of key factors involved in MAPK signaling pathways.

Results: EGFL6 displayed no cytotoxicity and was capable of promoting cell migration and angiogenesis. Besides, EGFL6 enhanced the mineralization process and up-regulated the expression levels of odontoblastic-related markers (DSPP, DMP1, and BSP) after 5, 7, and 10 days. The expression levels of odontoblastic-related and angiogenesis-related proteins (DSPP, DMP1, VEGF, and ALP) could all be up-regulated by EGFL6. There was also an increase in the phosphorylation levels of ERK1/2 and P38.

Conclusion: EGFL6 can promote the migration, angiogenesis, and odontogenesis differentiation of DPSCs via the activation of MAPK signaling pathways.

Since the authors are not responding to the editor’s requests to fulfill the editorial requirement, therefore, the article has been withdrawn from the journal Current Stem Cell Research & Therapy.

The Publisher apologizes to the readers of the journal for any inconvenience this may have caused.

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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.

Aims: The aim of this study was to investigate the role of human umbilical cord mesenchymal stem cell-derived exosomes (hUCMSC-Exo) in regulating the intestinal type 2 immune response for either protection or therapy.

Background: hUCMSC-Exo was considered a novel cell-free therapeutic product that shows promise in the treatment of various diseases. Type 2 immunity is a protective immune response classified as T-helper type 2 (Th2) cells and is associated with helminthic infections and allergic diseases. The effect of hUCMSC-Exo on intestinal type 2 immune response is not clear.

Method: C57BL/6 mice were used to establish intestinal type 2 immune response by administering of H. poly and treated with hUCMSC-Exo before or after H. poly infection. Intestinal organoids were isolated and co-cultured with IL-4 and hUCMSC-Exo. Then, we monitored the influence of hUCMSC-Exo on type 2 immune response by checking adult worms, the hyperplasia of tuft and goblet cells Result: hUCMSC-Exo significantly delays the colonization of H. poly in subserosal layer of duodenum on day 7 post-infection and promotes the hyperplasia of tuft cells and goblet cells on day 14 post-infection. HUCMSC-Exo enhances the expansion of tuft cells in IL-4 treated intestinal organoids, and promotes lytic cell death.

Conclusion: Our study demonstrates hUCMSC-Exo may benefit the host by increasing the tolerance at an early infection stage and then enhancing the intestinal type 2 immune response to impede the helminth during Th2 priming. Our results show hUCMSC-Exo may be a positive regulator of type 2 immune response, suggesting hUCMSC-Exo has a potential therapeutic effect on allergic diseases.

Alzheimer's disease (AD), an inexorable neurodegenerative ailment marked by cognitive impairment and neuropsychiatric manifestations, stands as the foremost prevailing form of dementia in the geriatric population. Its pathological signs include the aggregation of amyloid proteins, hyperphosphorylation of tau proteins, and the consequential loss of neural cells. The etiology of AD has prompted the formulation of numerous conjectures, each endeavoring to elucidate its pathogenesis. While a subset of therapeutic agents has displayed clinical efficacy in AD patients, a significant proportion has encountered disappointment. Notably, the extent of neural cell depletion bears a direct correlation with the disease's progressive severity. However, the absence of efficacious therapeutic remedies for neurodegenerative afflictions engenders a substantial societal burden and exerts a notable economic toll. In the past two decades, the realm of regenerative cell therapy, referred to as stem cell therapy, has unfolded as an avenue for the exploration of profoundly innovative approaches to treat neurodegenerative conditions. This promise is underpinned by the remarkable capacity of stem cells to remediate compromised neural tissue by means of cell replacement, to cultivate an environment conducive to regeneration, and to shield extant healthy neuronal and glial components from further degradation. Thus, this review aims to delve into the current knowledge of stem cell-based therapies and future possibilities in this domain.