scholarly journals GW29-e0135 Astrocytic endothelin-1 overexpression promotes neural progenitor cells proliferation and differentiation into astrocytes via the Jak2/Stat3 pathway after stroke

2018 ◽  
Vol 72 (16) ◽  
pp. C77
Author(s):  
Xiao Cheng ◽  
Patrick KK. Yeung ◽  
Sookja Kim Chung
2011 ◽  
Vol 46 (1) ◽  
pp. 325-332 ◽  
Author(s):  
Marion N. Schölzke ◽  
Amely Röttinger ◽  
Sasidhar Murikinati ◽  
Nadine Gehrig ◽  
Christoph Leib ◽  
...  

2020 ◽  
Vol 530 (1) ◽  
pp. 209-214 ◽  
Author(s):  
Yang Xu ◽  
Karolina Hajdukiewicz ◽  
Anshul Tiwari ◽  
Joanna Przybyś ◽  
Jan Rodriguez Parkitna ◽  
...  

2017 ◽  
Vol 127 (3) ◽  
pp. 490-501 ◽  
Author(s):  
Hui Qiao ◽  
Yun Li ◽  
Zhendong Xu ◽  
Wenxian Li ◽  
Zhijian Fu ◽  
...  

Abstract Background In human cortical neural progenitor cells, we investigated the effects of propofol on calcium homeostasis in both the ryanodine and inositol 1,4,5-trisphosphate calcium release channels. We also studied propofol-mediated effects on autophagy, cell survival, and neuro- and gliogenesis. Methods The dose–response relationship between propofol concentration and duration was studied in neural progenitor cells. Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and lactate dehydrogenase release assays. The effects of propofol on cytosolic calcium concentration were evaluated using Fura-2, and autophagy activity was determined by LC3II expression levels with Western blot. Proliferation and differentiation were evaluated by bromodeoxyuridine incorporation and immunostaining with neuronal and glial markers. Results Propofol dose- and time-dependently induced cell damage and elevated LC3II expression, most robustly at 200 µM for 24 h (67 ± 11% of control, n = 12 to 19) and 6 h (2.4 ± 0.5 compared with 0.6 ± 0.1 of control, n = 7), respectively. Treatment with 200 μM propofol also increased cytosolic calcium concentration (346 ± 71% of control, n = 22 to 34). Propofol at 10 µM stimulated neural progenitor cell proliferation and promoted neuronal cell fate, whereas propofol at 200 µM impaired neuronal proliferation and promoted glial cell fate (n = 12 to 20). Cotreatment with ryanodine and inositol 1,4,5-trisphosphate receptor antagonists and inhibitors, cytosolic Ca2+ chelators, or autophagy inhibitors mostly mitigated the propofol-mediated effects on survival, proliferation, and differentiation. Conclusions These results suggest that propofol-mediated cell survival or neurogenesis is closely associated with propofol’s effects on autophagy by activation of ryanodine and inositol 1,4,5-trisphosphate receptors.


2007 ◽  
Vol 120 (8) ◽  
pp. 1358-1370 ◽  
Author(s):  
J.-Y. Joo ◽  
B.-W. Kim ◽  
J.-S. Lee ◽  
J.-Y. Park ◽  
S. Kim ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Maria Maddalena Valente ◽  
Megan Allen ◽  
Valeria Bortolotto ◽  
Seung T. Lim ◽  
Katherine Conant ◽  
...  

Matrix metalloproteinases (MMPs) are zinc-dependent endopeptidases that play a role in varied forms of developmental and postnatal neuroplasticity. MMP substrates include protease-activated receptor-1 (PAR-1), a G-protein coupled receptor expressed in hippocampus. We examined proliferation and differentiation of adult neural progenitor cells (aNPCs) from hippocampi of mice that overexpress the potent PAR-1 agonist MMP-1. We found that, as compared to aNPCs from littermate controls, MMP-1 tg aNPCs display enhanced proliferation. Under differentiating conditions, these cells give rise to a higher percentage of MAP-2+neurons and a reduced number of oligodendrocyte precursors, and no change in the number of astrocytes. The fact that these results are MMP and PAR-1 dependent is supported by studies with distinct antagonists. Moreover, JSH-23, an inhibitor of NF-κB p65 nuclear translocation, counteracted both the proliferation and differentiation changes seen in MMP-1 tg-derived NPCs. In complementary studies, we found that the percentage of Sox2+undifferentiated progenitor cells is increased in hippocampi of MMP-1 tg animals, compared to wt mice. Together, these results add to a growing body of data suggesting that MMPs are effectors of hippocampal neuroplasticity in the adult CNS and that the MMP-1/PAR-1 axis may play a role in neurogenesis following physiological and/or pathological stimuli.


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