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Literature Updates. For Members. For Librarians. RSS Feeds. Chemistry World. Education in Chemistry. Open Access. Historical Collection. You do not have JavaScript enabled. Please enable JavaScript to access the full features of the site or access our non-JavaScript page. Volume 26, Harms et al. By in vivo and in vitro studies using the rat model, Jeanneteau et al. In any case, neuroprotective pathways in postmitotic neurons prevent new cell cycles. We demonstrated that GCs differently stimulate the proliferation of MAP2-positive neurons under oxidative stress.

As described above, it has been reported that GR suppresses cell proliferation and causes apoptosis. In the present study, the GCs showed similar effects under non-stressed conditions. This may suggest that the activation of MR plays an important role in the proliferation of neurons under oxidative stress. Another possibility could be the difference in the inactivation mechanisms of the GCs.

Thus, the continuous GR activity may induce apoptosis under stress conditions. Halliday et al. Further clinical and mechanistic studies are required to determine the optimal choice of GCs for children with CLD. Further mechanistic studies are needed to reveal how GCs induce NPC proliferation and how oxidative stress modulates the effects of GCs.

Brain Res , Pediatr Res , Cell Death Dis , 1: e J Pediatr , Nat Biotechnol , Int J Pediatr , Endocr Rev , Google Scholar. In J Neurosci , In Exp Neurol , Adv Exp Med Biol , J Clin Invest , Antioxid Redox Signal , Am J Obstet Gynecol , In Toxicol Sci , Pediatrics , Neurobiol Dis , Nat Methods , 9: Neuron , 2: N Engl J Med , Download references. We thank Dr Katherine E Santostefano University of Florida for helpful discussion and critical readings of the manuscript.

Correspondence to Haruo Shintaku. MT, AU provided materials and conceived of the study. HS participated in study design, coordination and helped to draft the manuscript. All authors read and approved the final manuscript.

Reprints and Permissions. Ninomiya, E. Glucocorticoids promote neural progenitor cell proliferation derived from human induced pluripotent stem cells. SpringerPlus 3, Download citation. Received : 25 July Accepted : 06 September Published : 15 September Skip to main content. Search all SpringerOpen articles Search. Download PDF. Abstract Glucocorticoids GCs are frequently used for treating and preventing chronic lung disease and circulatory dysfunction in premature infants.

Introduction In recent years, systemic glucocorticoids GCs have frequently been administered to treat and prevent chronic lung disease CLD , which is also known as bronchopulmonary dysplasia, and circulatory dysfunction in premature infants. Human iPS cell culture and neural progenitor cells induction The study was approved by the Ethics Committees of the Osaka City University approval and was conducted according to the declaration of Helsinki.

Results GC treatment promoted neural progenitor cell proliferation To evaluate the effect of GCs on the proliferation of NPCs, we initially performed a cell proliferation assay. Figure 1. Full size image. Figure 2. Figure 3. Figure 4.

Cell cycle regulation induced by GCs Samarasinghe et al. Neuroprotective effects of GCs GCs exhibit protective effects on postmitotic neurons. Differential mechanisms of action between GCs We demonstrated that GCs differently stimulate the proliferation of MAP2-positive neurons under oxidative stress.

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