ABSTRACT
Objective@#The heart contains a pool of c-kit+ progenitor cells which is believed to be able to regenerate. The differentiation of these progenitor cells is reliant on different physiological cues. Unraveling the underlying signals to direct differentiation of progenitor cells will be beneficial in controlling progenitor cell fate. In this regard, the role of the mitochondria in mediating cardiac progenitor cell fate remains unclear. Specifically, the association between changes in mitochondrial morphology with the differentiation status of c-kit+ CPCs remains elusive. In this study, we investigated the relationship between mitochondrial morphology and the differentiation status of c-kit+ progenitor cells. @*Methods@#and Results: c-kit+ CPCs were isolated from 2-month-old male wild-type FVB mice. To activate differentiation, CPCs were incubated in α-minimal essential medium containing 10 nM dexamethasone for up to 7 days. To inhibit Drp1-mediated mitochondrial fragmentation, either 10 μM or 50 μM mdivi-1 was administered once at Day 0 and again at Day 2 of differentiation. To inhibit calcineurin, either 1 μM or 5 μM ciclosporin-A (CsA) was administered once at Day 0 and again at Day 2 of differentiation. Dexamethasone-induced differentiation of c-kit+ progenitor cells is aligned with fragmentation of the mitochondria via a calcineurin-Drp1 pathway. Pharmacologically inhibiting mitochondrial fragmentation retains the undifferentiated state of the c-kit+ progenitor cells. @*Conclusions@#The findings from this study provide an alternative view of the role of mitochondrial fusion-fission in the differentiation of cardiac progenitor cells and the potential of pharmacologically manipulating the mitochondria to direct progenitor cell fate.
ABSTRACT
Radiation safety has been a focus of attention in the past few years. This review summarizes the researches related to the effective dose (ED) of PET/CT in recent years, including the ranges and influential factors of ED. In order to provide guidance in clinical practice, the common methods for estimating ED of PET/CT are also introduced.
ABSTRACT
The radioactive iodine-refractory differentiated thyroid carcinoma (RIR-DTC) is a complex process that involves multiple genetic changes and multiple signaling pathways.Radionuclide imaging, genomics and proteomics are effective to clarify the mechanism and helpful in clinical diagnosis and therapy.The treatment of RIR-DTC includes the removal of distant metastases, drug therapy, external radiotherapy and radiofrequency ablation.This review mainly focuses on the pathogenesis, diagnosis and treatment of RIR-DTC.
ABSTRACT
Interleukin 7 receptor (IL7R) is a transmembrane receptor that belongs to the typeⅠcytokine receptor fami-ly. It consists of the cytokine-specific α-chain (IL7Rα, CD127) and the shared common cytokine γ-chain (γc, CD132). IL-7R is expressed in various cell types, including lymphoid precursor cells, pro-B cells, T cells, thymocytes, dendritic cells, myeloid cells and monocytes. Under physiological conditions, IL7R is a vital cytokine for development and survival of T and B cells. IL7R plays a key role in the pathogenesis of multiple sclerosis (MS). Single nucleotide polymorphisms (SNPs) in the gene encoding IL7Rαhave emerged through genetic studies of MS patients. In experimental autoimmune encephalomy-elitis (EAE) mouse model of MS, treatment with neutralizing anti-IL7Rαantibody results in significant improvement of EAE. Therefore, IL7R may serve as a novel target for MS therapies.
ABSTRACT
Tumor necrosis factor (TNF)-αis a pleiotropic inflammatory cytokine, which is produced chiefly by acti?vated macrophages. Two forms of TNF-α, soluble and transmembrane, can bind tumor necrosis factor receptor (TNFR) 1 or TNFR2, respectively. Recently, a concept has emerged that TNF-α/TNFR pathway plays an important role in the pathogene?sis of multiple sclerosis and remyelination. TNFR1 induces death of oligodendrocytes via death receptor-mediated apoptosis, which leads to demyelination or other neurodegenerative changes. However, TNFR2 has a positive effect on multiple sclero?sis. It facilitates the proliferation and differentiation of oligodendrocyte precursor cells, thus promoting remyelination.