Regulation of pituitary adenylate cyclase activating polypeptide and its receptor type 1 after traumatic brain injury: comparison with brain-derived neurotrophic factor and the induction of neuronal cell death

Neuroscience ◽  
1999 ◽  
Vol 90 (1) ◽  
pp. 235-247 ◽  
Author(s):  
Y Skoglösa ◽  
A Lewén ◽  
N Takei ◽  
L Hillered ◽  
D Lindholm
2008 ◽  
Vol 25 (7) ◽  
pp. 755-767 ◽  
Author(s):  
Roya Tehranian ◽  
Marie E. Rose ◽  
Vincent Vagni ◽  
Alicia M. Pickrell ◽  
Raymond P. Griffith ◽  
...  

Author(s):  
Xingyun Quan ◽  
Li Song ◽  
Xiaomei Zheng ◽  
Shenjie Liu ◽  
Huaqiang Ding ◽  
...  

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Zhongyuan Bao ◽  
Yinlong Liu ◽  
Binglin Chen ◽  
Zong Miao ◽  
Yiming Tu ◽  
...  

AbstractProkineticin-2 (Prok2) is an important secreted protein likely involved in the pathogenesis of several acute and chronic neurological diseases through currently unidentified regulatory mechanisms. The initial mechanical injury of neurons by traumatic brain injury triggers multiple secondary responses including various cell death programs. One of these is ferroptosis, which is associated with dysregulation of iron and thiols and culminates in fatal lipid peroxidation. Here, we explore the regulatory role of Prok2 in neuronal ferroptosis in vitro and in vivo. We show that Prok2 prevents neuronal cell death by suppressing the biosynthesis of lipid peroxidation substrates, arachidonic acid-phospholipids, via accelerated F-box only protein 10 (Fbxo10)-driven ubiquitination, degradation of long-chain-fatty-acid-CoA ligase 4 (Acsl4), and inhibition of lipid peroxidation. Mice injected with adeno-associated virus-Prok2 before controlled cortical impact injury show reduced neuronal degeneration and improved motor and cognitive functions, which could be inhibited by Fbxo10 knockdown. Our study shows that Prok2 mediates neuronal cell deaths in traumatic brain injury via ferroptosis.


2012 ◽  
Vol 218 (1) ◽  
pp. 209-220 ◽  
Author(s):  
Tatsuki Itoh ◽  
Motohiro Imano ◽  
Shozo Nishida ◽  
Masahiro Tsubaki ◽  
Nobuyuki Mizuguchi ◽  
...  

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