Article of the Year 2021
Combined Use of Chitosan and Olfactory Mucosa Mesenchymal Stem/Stromal Cells to Promote Peripheral Nerve Regeneration In VivoRead the full article
Stem Cells International publishes papers in all areas of stem cell biology and applications. The journal publishes basic, translational, and clinical research, including animal models and clinical trials.
Chief Editor Professor Li has a background in cardiac stem cell transplantation, using young stem cells to promote tissue repair following injury to rejuvenate the aged individual, and the development of biomaterials that can easily integrate into damaged heart tissue.
Latest ArticlesMore articles
Autophagy Regulates Osteogenic Differentiation of Human Periodontal Ligament Stem Cells Induced by Orthodontic Tension
Tooth movement is the core of orthodontics. Osteogenesis of the tension side under orthodontic force has great significance on tooth movement and stability, which involves complex mechanical and biological signal transduction. However, the mechanism remains unclear. Through in vitro cell studies, we observed the increased expression levels of osteogenesis-related factors and autophagy-related factors during the osteogenic differentiation of mesenchymal stem cells induced by orthodontic force. The change trend of autophagy-related factors and osteogenesis-related factors is similar, which indicates the involvement of autophagy in osteogenesis. In the study of autophagy-related gene ATG7 silenced cells, the expression level of autophagy was significantly inhibited, and the expression level of osteogenesis-related factors also decreased accordingly. Through drug regulation, we observed that the increase of autophagy level could effectively promote osteogenic differentiation, while the decrease of the autophagy level inhibited this process to some extent. Therefore, autophagy plays an important role in the osteogenic differentiation of mesenchymal stem cells induced by orthodontic force, which provides a novel idea useful for orthodontic treatment in promoting periodontal tissue remodeling and accelerating tooth movement.
Characterizing the Crosstalk of NCAPG with Tumor Microenvironment and Tumor Stemness in Stomach Adenocarcinoma
Background. Nonstructural maintenance of non-SMC condensin I complex subunit G (NCAPG) exerts critical effects on cancer progression. However, its biological roles in tumorigenesis and metastasis remain unclear. Thus, we aimed to assess the prognostic utility of NCAPG in stomach adenocarcinoma (STAD) and its potential as a tumor biomarker. Methods. Pan-cancer expression profile dataset from public databases and corresponding clinical information were extracted. Single-sample gene set enrichment analysis (ssGSEA) was performed for the evaluation of immune correlations pan-cancer. Subsequently, we focused on STAD and evaluated the methylation profiles, copy number variants (CNVs), and single nucleotide variants (SNVs). Immune features were analyzed between high and low NCAPG expression groups. Differential analysis was performed between high and low expression groups to identify differentially expressed genes (DEGs). Prognostic DEGs were screened by univariate analysis, and an NCAPG-based risk model was constructed based on the prognostic DEGs and LASSO analysis. Results. NCAPG expression in STAD was significantly and positively correlated with four immune checkpoints, namely, CTLA4, PDCD1, LAG3, and CD276, but was negatively correlated with the infiltration of most immune cells. High and low NCAPG expression groups had differential overall survival, tumor mutation burden, and differential enrichment of therapeutic-related pathways. An immune risk scoring model related to NCAPG expression and immune score was constructed which showed a favorable performance in predicting STAD prognosis as well as predicting the response to immunotherapy. In addition, we found a higher mRNA stemness index (mRNAsi) in the high-risk group and a positive correlation between NCAPG expression and mRNAsi. Conclusion. NCAPG was suggested to be involved in the regulation of tumor microenvironment in STAD. High NCAPG expression was related to high tumor stemness and good prognosis. The immune risk model had a potential to predict STAD prognosis and help directing therapeutic treatment.
Mesenchymal Stem Cells May Alleviate the Intervertebral Disc Degeneration by Reducing the Oxidative Stress in Nucleus Pulposus Cells
Background. Stem cell therapy is a promising therapeutic modality for intervertebral disc degeneration (IDD). Oxidative stress is a vital contributor to the IDD; however, the definite role of oxidative stress in stem cell therapy for IDD remains obscure. The aim of this study was to determine the vital role of oxidative stress-related differentially expressed genes (OSRDEGs) in degenerative NPCs cocultured with mesenchymal stem cells (MSCs). Methods. A series of bioinformatic methods were used to calculate the oxidative stress score and autophagy score, identify the OSRDEGs, conduct the function enrichment analysis and protein-protein interaction (PPI) analysis, build the relevant competing endogenous RNA (ceRNA) regulatory networks, and explore the potential association between oxidative stress and autophagy in degenerative NPCs cocultured with MSCs. Results. There was a significantly different oxidative stress score between NPC/MSC samples and NPC samples (). Forty-one OSRDEGs were selected for the function enrichment and PPI analyses. Ten hub OSRDEGs were obtained according to the PPI score, including JUN, CAT, PTGS2, TLR4, FOS, APOE, EDN1, TXNRD1, LRRK2, and KLF2. The ceRNA regulatory network, which contained 17 DElncRNAs, 240 miRNAs, and 10 hub OSRDEGs, was constructed. Moreover, a significant relationship between the oxidative stress score and autophagy score was observed (), and 125 significantly related gene pairs were obtained (, ). Conclusion. Stem cell therapy might repair the degenerative IVD via reducing the oxidative stress through the ceRNA regulatory work and restoration of autophagy in degenerative NPCs. This research could provide new insights into the mechanism research of stem cell therapy for IDD and potential therapeutic targets in the IDD treatment.
FAIM Enhances the Efficacy of Mesenchymal Stem Cell Transplantation by Inhibiting JNK-Induced c-FLIP Ubiquitination and Degradation
Background. The poor survival rates of transplanted mesenchymal stem cells (MSCs) in harsh microenvironments impair the efficacy of MSCs transplantation in myocardial infarction (MI). Extrinsic apoptosis pathways play an important role in the apoptosis of transplanted MSCs, and Fas apoptosis inhibitory molecule (FAIM) is involved in regulation of the extrinsic apoptosis pathway. Thus, we aimed to explore whether FAIM augmentation protects MSCs against stress-induced apoptosis and thereby improves the therapeutic efficacy of MSCs. Methods. We ligated the left anterior descending coronary artery (LAD) in the mouse heart to generate an MI model and then injected FAIM-overexpressing MSCs (MSCsFAIM) into the peri-infarction area in vivo. Moreover, FAIM-overexpressing MSCs were challenged with oxygen, serum, and glucose deprivation (OGD) in vitro, which mimicked the harsh microenvironment that occurs in cardiac infarction. Results. FAIM was markedly downregulated under OGD conditions, and FAIM overexpression protected MSCs against OGD-induced apoptosis. MSCsFAIM transplantation improved cell retention, strengthened angiogenesis, and ameliorated heart function. The antiapoptotic effect of FAIM was mediated by cellular-FLICE inhibitory protein (c-FLIP), and FAIM augmentation improved the protein expression of c-FLIP by reducing ubiquitin–proteasome-dependent c-FLIP degradation. Furthermore, FAIM inhibited the activation of JNK, and treatment with the JNK inhibitor SP600125 abrogated the reduction in c-FLIP protein expression caused by FAIM silencing. Conclusions. Overall, these results indicated that FAIM curbed the JNK-mediated, ubiquitination–proteasome-dependent degradation of c-FLIP, thereby improving the survival of transplanted MSCs and enhancing their efficacy in MI. This study may provide a novel approach to strengthen the therapeutic effect of MSC-based therapy.
The Diagnostic Value of Bedside Echocardiography and Lower Extremity Blood Vessels in Acute Pulmonary Embolism
Objective. The study aimed to evaluate the value of bedside echocardiography (TTE) and lower extremity blood vessels in diagnosis and prognosis of acute pulmonary embolism (APE). Methods. A retrospective study was performed on 53 patients with APE diagnosed by CT pulmonary angiography (CTPA) (systemic systolic blood pressure was >90 mmHg at time of consultation, and systemic systolic blood pressure decreased by <40 mmHg compared with basic value in those with hypertension). All patients underwent TTE examination before treatment. The high-risk factors, clinical manifestations, laboratory tests, and prognosis were retrospectively analyzed. Results. The rate of PE-related deterioration (cardiopulmonary resuscitation, tracheal intubation, cardiogenic shock, and death) within 14 days of hospitalization in RVD was 28%, and mortality rate (sudden death) was 20%, compared with non-RVD (both 0%). TTE examination showed that RVD as a predictor of pulmonary embolism-related death had a sensitivity of 100%, a specificity of 58%, a positive predictive value of 20%, and a negative predictive value of 100%. Conclusions. (1) TTE has increasingly shown obvious advantages in diagnosis of APE. It can detect direct or indirect signs of pulmonary embolism, confirm diagnosis or suspected diagnosis, and noninvasively and dynamically observe hemodynamic changes of heart in patients with acute PTE before and after treatment.. (2) The PE-related exacerbation rate (28%) or mortality (20%) of APE patients in normotensive with RVD was higher without RVD (0%). RVD is an independent predictor of poor prognosis in normotensive acute PTE. TTE tests allow people to identify people at risk of early death. The short-term prognosis of patients without RVD was better (14 days).
Effects of Exercise or Mechanical Stimulation on Bone Development and Bone Repair
The development and regeneration of the bone are tightly regulated by mechanical cues. Multiple cell types, including osteoblasts, osteocytes, osteoclasts, mesenchymal stem cells (MSCs), and recently found skeletal stem cells (SSCs), are responsible for efficient bone development and injury repair. The immune cells in the environment interact with bone cells to maintain homeostasis and facilitate bone regeneration. Investigation of the mechanism by which these cells sense and respond to mechanical signals in bone is fundamental for optimal clinical intervention in bone injury healing. We discuss the effects of exercise programs on fracture healing in animal models and human patients, which encouragingly suggest that carefully designed exercise prescriptions can improve the result of fracture healing during the remodeling phase. However, additional clinical tracing and date accumulation are still required for the pervasive application of exercise prescriptions to improve fracture healing.