scholarly journals Extracellular ATP signaling and homeostasis in plant cells

2012 ◽  
Vol 7 (5) ◽  
pp. 566-569 ◽  
Author(s):  
Jian Sun ◽  
Chunlan Zhang ◽  
Xuan Zhang ◽  
Shurong Deng ◽  
Rui Zhao ◽  
...  

2021 ◽  
Author(s):  
Ha N. Duong ◽  
Sung‐Hwan Cho ◽  
Limin Wang ◽  
An Q. Pham ◽  
Julia M. Davies ◽  
...  


2013 ◽  
Vol 702 (1-3) ◽  
pp. 242-249 ◽  
Author(s):  
Hector Zerpa ◽  
Carol Crawford ◽  
Gillian E. Knight ◽  
Alice F. Fordham ◽  
Silvia E. Janska ◽  
...  


2019 ◽  
Vol 317 (1) ◽  
pp. E25-E41 ◽  
Author(s):  
Clarissa Bartley ◽  
Thierry Brun ◽  
Lucie Oberhauser ◽  
Mariagrazia Grimaldi ◽  
Filippo Molica ◽  
...  

Fructose is widely used as a sweetener in processed food and is also associated with metabolic disorders, such as obesity. However, the underlying cellular mechanisms remain unclear, in particular, regarding the pancreatic β-cell. Here, we investigated the effects of chronic exposure to fructose on the function of insulinoma cells and isolated mouse and human pancreatic islets. Although fructose per se did not acutely stimulate insulin exocytosis, our data show that chronic fructose rendered rodent and human β-cells hyper-responsive to intermediate physiological glucose concentrations. Fructose exposure reduced intracellular ATP levels without affecting mitochondrial function, induced AMP-activated protein kinase activation, and favored ATP release from the β-cells upon acute glucose stimulation. The resulting increase in extracellular ATP, mediated by pannexin1 (Panx1) channels, activated the calcium-mobilizer P2Y purinergic receptors. Immunodetection revealed the presence of both Panx1 channels and P2Y1 receptors in β-cells. Addition of an ectonucleotidase inhibitor or P2Y1 agonists to naïve β-cells potentiated insulin secretion stimulated by intermediate glucose, mimicking the fructose treatment. Conversely, the P2Y1 antagonist and Panx1 inhibitor reversed the effects of fructose, as confirmed using Panx1-null islets and by the clearance of extracellular ATP by apyrase. These results reveal an important function of ATP signaling in pancreatic β-cells mediating fructose-induced hyper-responsiveness.





2010 ◽  
Vol 20 (10) ◽  
pp. 601-608 ◽  
Author(s):  
Kiwamu Tanaka ◽  
Simon Gilroy ◽  
Alan M. Jones ◽  
Gary Stacey


2018 ◽  
Vol 188 ◽  
pp. 67-73 ◽  
Author(s):  
Lei Dou ◽  
Yi-Fa Chen ◽  
Peter J. Cowan ◽  
Xiao-Ping Chen


eNeuro ◽  
2020 ◽  
pp. ENEURO.0185-20.2020
Author(s):  
Matthias Ollivier ◽  
Juline Beudez ◽  
Nathalie Linck ◽  
Thomas Grutter ◽  
Vincent Compan ◽  
...  


2006 ◽  
Vol 290 (1) ◽  
pp. C27-C34 ◽  
Author(s):  
Yan Sun ◽  
Toby C. Chai

Interstitial cystitis (IC) is an idiopathic hypersensory condition of the bladder associated with increased urinary ATP and increased stretch-activated ATP release by bladder urothelial cells (BUCs), suggesting augmented purinergic signaling in the bladder. To test this theory further, monolayers of cultured BUCs derived from bladder biopsies obtained from patients with IC and control patients were stimulated with 10–30 μM ATP with subsequent measurement of extracellular ATP levels using the luciferin-luciferase assay. Stimulation with 30 μM ATP resulted in IC supernatant containing several-fold more ATP than control BUCs initially, followed by a slower decrease in ATP levels. This difference in ATP levels was not completely due to activity of cellular ecto-ATPase, because blockade with ARL67156 did not normalize the difference. Exposure to hypotonic solutions resulted in similar extracellular ATP concentrations in IC and control BUCs, but there was a slower decrease in ATP levels in IC supernatants. Treatment of IC BUCs with 10–40 μM suramin, a nonspecific P2 receptor antagonist, significantly attenuated the IC BUC response to extracellular ATP, restoring IC BUCs to a control phenotype. Pretreatment of IC BUCs with 20 ng/ml of heparin-binding EGF-like growth factor (HB-EGF), which previously has been shown to be decreased in IC urine specimens, also restored IC BUCs to a control phenotype with respect to response to ATP stimulation. In conclusion, IC BUCs have augmented extracellular ATP signaling that could be blocked by suramin and HB-EGF. These findings suggest the possible development of future novel therapeutic techniques.



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