Electrochemical quantification of transmitter concentration in single nanoscale vesicles isolated from PC12 cells

2018 ◽  
Vol 210 ◽  
pp. 353-364 ◽  
Author(s):  
Xianchan Li ◽  
Johan Dunevall ◽  
Andrew G. Ewing
Keyword(s):  
Pc12 Cells ◽  
Electrochemical Cytometry ◽  
Catecholamine Concentration

Vesicle impact electrochemical cytometry shows vesicular catecholamine concentration is relatively constant and independent of the vesicular size.

The influence of DHEA on NGF-induced differentiation of pheochromocytoma PC12 cells

2006 ◽  
Vol 114 (S 1) ◽  
Author(s):  
CG Ziegler ◽  
AW Krug ◽  
F Sicard ◽  
S Sperber ◽  
M Ehrhart-Bornstein ◽  
...  
Keyword(s):  
Pc12 Cells ◽  
Induced Differentiation ◽  
Pheochromocytoma Pc12 ◽  
Pheochromocytoma Pc12 Cells

Hyperforin mediates neurite outgrowth via TRPC6 channels in PC12 cells

2007 ◽  
Vol 40 (05) ◽  
Author(s):  
K Leuner ◽  
M Müller ◽  
V Kasanzki ◽  
C Harteneck ◽  
WE Müller
Keyword(s):  
Neurite Outgrowth ◽  
Pc12 Cells

Irisin Ameliorates Hypoxia/Reoxygenation-Induced Inflammation and Apoptosis in PC12 Cells by Inhibiting TLR4/MYD88 Signaling Pathway

2019 ◽  
Vol 17 (3) ◽  
pp. 329-336
Author(s):  
Wang Jinli ◽  
Xu Fenfen ◽  
Zheng Yuan ◽  
Cheng Xu ◽  
Zhang Piaopiao ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Signaling Pathway ◽  
Pc12 Cells ◽  
Major Complication ◽  
Lactic Dehydrogenase ◽  
Dependent Manner ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic ◽  
Myd88 Signaling ◽  
Hypoxia Reoxygenation

Cardiovascular disease including cerebral ischemic stroke is the major complication that increases the morbidity and mortality in patients with diabetes mellitus as much as four times. It has been well established that irisin, with its ability to regulate glucose and lipid homeostasis as well as anti-inflammatory and anti-apoptotic properties, has been widely examined for its therapeutic potentials in managing metabolic disorders. However, the mechanism of irisin in the regulation of cerebral ischemic stroke remains unclear. Using PC12 cells as a model, we have shown that hypoxia/reoxygenation inhibits cell viability and increases lactic dehydrogenase. Irisin, in a dose-dependent manner, reversed these changes. The increase in inflammatory mediators (IL-1β, IL-6, and TNF-α) by hypoxia/reoxygenation was reversed by irisin. Furthermore, the cell apoptosis promoted by hypoxia/reoxygenation was also inhibited by irisin. Irisin suppressed TLR4/MyD88 signaling pathway leading to amelioration of inflammation and apoptosis in PC12 cells. Thus, inhibition of TLR4/MyD88 signaling pathway via irisin could be an important mechanism in the regulation of hypoxia/reoxygenation-induced inflammation and apoptosis in PC12 cells.

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