Regeneration of damaged brain tissue with neural stem cells is a promising strategy for reversing neurologic deficits.¹ Superparamagnetic iron oxide nanoparticles have been used to label and track dendritic cells in the experimental treatment of melanoma² and in experiments in animals.³ We report the feasibility of labeling neural stem cells from humans (two patients for whom written informed consent was provided by next of kin) with superparamagnetic iron oxide nanoparticles and tracking them with the use of magnetic resonance imaging (MRI).

Cancer stem‐like cells, which have been described as tumor‐initiating cells or tumor‐propagating cells, play a crucial role in our fundamental understanding of glioblastoma multiforme (GBM) and its recurrence. GBM is a lethal cancer, characterized by florid vascularization and aberrantly elevated vascular endothelial growth factor (VEGF). VEGF promotes tumorigenesis and angiogenesis of human GBM stem‐like cells (GBSCs). However, whether and how VEGF contributes to GBSCs proliferation remain largely uncertain. In this study, human GBSCs were isolated from surgical specimens of glioblastoma and cultured in medium favored for stem cell growth. Neural Colony‐Forming Cell Assay and ATP assay were performed to measure GBSC proliferation under normoxia (20% O₂) and hypoxia (1% O₂). Our observations demonstrate that exogenous VEGF stimulates GBSC proliferation in a dose‐dependent manner via VEGF Receptor 2 (VEGFR2); while VEGF Receptor 1 (VEGFR1) has a negative feedback effect on VEGFR2 when cells were exposed to higher concentration of VEGF. These results suggest that suppressing VEGFR2‐dependent GBSC proliferation is a potentially therapeutic strategy in GBM.

Stroke is a major disease that leads to high mortality and morbidity. Given the ageing population and the potential risk factors, the prevalence of stroke and socioeconomic burden associated with stroke are expected to increase. During the past decade, both prophylactic and therapeutic strategies for stroke have made significant progress. However, current therapies still cannot adequately improve the outcomes of stroke and may not apply to all patients. One of the significant advances in modern medicine is cell-derived neurovascular regeneration and neuronal repair. Progress in stem cell biology has greatly contributed to ameliorating stroke-related brain injuries in preclinical studies and demonstrated clinical potential in stroke treatment. Mesenchymal stem cells (MSCs) have the differentiating potential of chondrocytes, adipocytes, and osteoblasts, and they have the ability to transdifferentiate into endothelial cells, glial cells, and neurons. Due to their great plasticity, MSCs have drawn much attention from the scientific community. This review will focus on MSCs, stem cells widely utilized in current medical research, and evaluate their effect and potential of improving outcomes in ischemic stroke.

Background. Mitochondrial dysfunctions play a pivotal role in cerebral ischemia‐reperfusion (I/R) injury. Although mitochondrial transplantation has been recently explored for the treatment of cerebral I/R injury, the underlying mechanisms and fate of transplanted mitochondria are still poorly understood. Methods. Mitochondrial morphology and function were assessed by fluorescent staining, electron microscopy, JC‐1, PCR, mitochondrial stress testing, and metabolomics. Therapeutic effects of mitochondria were evaluated by cell viability, reactive oxygen species (ROS), and apoptosis levels in a cellular hypoxia‐reoxygenation model. Rat middle cerebral artery occlusion model was applied to assess the mitochondrial therapy in vivo. Transcriptomics was performed to explore the underlying mechanisms. Mitochondrial fate tracking was implemented by a variety of fluorescent labeling methods. Results. Neuro‐2a (N2a) cell‐derived mitochondria had higher mitochondrial membrane potential, more active oxidative respiration capacity, and less mitochondrial DNA copy number. Exogenous mitochondrial transplantation increased cellular viability in an oxygen‐dependent manner, decreased ROS and apoptosis levels, improved neurobehavioral deficits, and reduced infarct size. Transcriptomic data showed that the differential gene enrichment pathways are associated with metabolism, especially lipid metabolism. Mitochondrial tracking indicated specific parts of the exogenous mitochondria fused with the mitochondria of the host cell, and others were incorporated into lysosomes. This process occurred at the beginning of internalization and its efficiency is related to intercellular connection. Conclusions. Mitochondrial transplantation may attenuate cerebral I/R injury. The mechanism may be related to mitochondrial component separation, altering cellular metabolism, reducing ROS, and apoptosis in an oxygen‐dependent manner. The way of isolated mitochondrial transfer into the cell may be related to intercellular connection.