NG2-expressing neural progenitor cells (i.e., NG2 glial cells) maintain their proliferative and migratory activities even in the adult mammalian central nervous system (CNS) and produce myelinating oligodendrocytes and astrocytes. Although NG2 glial cells have been observed in close proximity to neuronal cell bodies in order to receive synaptic inputs, substantive non-proliferative roles of NG2 glial cells in the adult CNS remain unclear. In the present study, we generated NG2-HSVtk transgenic rats and selectively ablated NG2 glial cells in the adult CNS. Ablation of NG2 glial cells produced defects in hippocampal neurons due to excessive neuroinflammation via activation of the interleukin-1 beta (IL-1β) pro-inflammatory pathway, resulting in hippocampal atrophy. Furthermore, we revealed that the loss of NG2 glial cell-derived hepatocyte growth factor (HGF) exacerbated these abnormalities. Our findings suggest that NG2 glial cells maintain neuronal function and survival via the control of neuroimmunological function.
Hair growth occurs periodically in a cycle that consists of three different phases: growth, regression, and resting. The length of each phase is regulated by both intrinsic and extrinsic factors throughout life, and influenced by physiological and pathological conditions. Elongation of the resting phase and shortening of the growth phase occur during physiological ageing and in baldness, respectively. In vivo discrimination of each phase of the hair cycle can be used to research for regeneration of hair follicles as well as to evaluate the efficacy of hair regrowth treatments in the same individual. Here we show that NG2+ epithelial cells in the hair follicles encompass bulge stem cells, and that the number of hair follicle NG2 cells underwent dramatic changes during the hair cycle. Transgenic rats with expression of firefly luciferase gene in NG2 cells were generated to monitor the hair cycle in vivo. Hair follicle NG2 cells were clearly visualized via bioluminescence imaging to study each phase of the hair cycle in the rats, from infancy to old age.
OBJECTIVEIn skeletal muscles, dantrolene inhibits the exercise-induced membrane translocation of GLUT4. It has been postulated that the inhibitory action of dantrolene on Ca2+ release from the sarcoplasmic reticulum (SR) causes inhibition of exercise-induced glucose uptake; however, the precise mechanism has not been adequately studied.RESEARCH DESIGN AND METHODSWe discovered that dantrolene can bind to skeletal-type neuroendocrine-specific protein-like 1 (sk-NSPl1) with photoreactive dantrolene derivatives. In sk-NSPl1–deficient muscles, we examined the change in glucose uptake and the membrane translocation of GLUT4. In addition, we examined the change in blood glucose and also measured the glycogen level in both isolated and in situ skeletal muscles after electrical stimulation using our mutant mouse.RESULTSIn sk-NSPl1–deficient muscles, exercise-induced glucose uptake was totally abolished with no change in insulin-induced glucose uptake. The Ca2+ release mechanism and its inhibition by dantrolene were completely preserved in these muscles. The expression of GLUT4 in the mutant muscles also appeared unchanged. Confocal imaging and results using the membrane isolation method showed that exercise/contraction did not enhance GLUT4 translocation in these sk-NSPl1–deficient muscles under conditions of adequate muscle glycogen consumption. The blood glucose level in normal mice was reduced by electrical stimulation of the hind limbs, but that in mutant mice was unchanged.CONCLUSIONSsk-NSPl1 is a novel dantrolene receptor that plays an important role in membrane translocation of GLUT4 induced by contraction/exercise. The 23-kDa sk-NSPl1 may also be involved in the regulation of glucose levels in the whole body.
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