scholarly journals Deficiency in the inner mitochondrial membrane peptidase 2-like (Immp21) gene increases ischemic brain damage and impairs mitochondrial function

2011 ◽  
Vol 44 (3) ◽  
pp. 270-276 ◽  
Author(s):  
Yi Ma ◽  
Suresh L. Mehta ◽  
Baisong Lu ◽  
P. Andy Li
Keyword(s):  
Brain Damage ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Inner Mitochondrial Membrane ◽  
Ischemic Brain Damage ◽  
Ischemic Brain

scholarly journals Deletion of Mitochondrial Uncoupling Protein-2 Increases Ischemic Brain Damage after Transient Focal Ischemia by Altering Gene Expression Patterns and Enhancing Inflammatory Cytokines

2010 ◽  
Vol 30 (11) ◽  
pp. 1825-1833 ◽  
Author(s):  
Bryan A Haines ◽  
Suresh L Mehta ◽  
Serena M Pratt ◽  
Craig H Warden ◽  
P Andy Li
Keyword(s):  
Brain Damage ◽  
Inflammatory Cytokines ◽  
Mitochondrial Membrane ◽  
Focal Ischemia ◽  
Wild Type ◽  
Inner Mitochondrial Membrane ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Transient Focal Ischemia

Mitochondrial hyperpolarization inhibits the electron transport chain and increases incomplete reduction of oxygen, enabling production of reactive oxygen species (ROS). The consequence is mitochondrial damage that eventually causes cell death. Uncoupling proteins (UCPs) are inner mitochondrial membrane proteins that dissipate the mitochondrial proton gradient by transporting H+ across the inner membrane, thereby stabilizing the inner mitochondrial membrane potential and reducing the formation of ROS. The role of UCP2 in neuroprotection is still in debate. This study seeks to clarify the role of UCP2 in transient focal ischemia (tFI) and to further understand the mechanisms of ischemic brain damage. Both wild-type and UCP2-knockout mice were subjected to tFI. Knocking out UCP2 significantly increased the infarct volume to 61% per hemisphere as compared with 18% in wild-type animals. Knocking out UCP2 suppressed antioxidant, cell-cycle, and DNA repair genes, including Sod1 and Sod2, Gstm1, and cyclins. Furthermore, knocking out UCP2 significantly upregulated the protein levels of the inflammatory cytokines, including CTACK, CXCL16, Eotaxin-2, fractalkine, and BLC. It is concluded that knocking out the UCP2 gene exacerbates neuronal death after cerebral ischemia with reperfusion and this detrimental effect is mediated by alteration of antioxidant genes and upregulation of inflammatory mediators.

scholarly journals Modulation of Mitochondrial Function and Autophagy Mediates Carnosine Neuroprotection Against Ischemic Brain Damage

Stroke ◽  
2014 ◽  
Vol 45 (8) ◽  
pp. 2438-2443 ◽  
Author(s):  
Seung-Hoon Baek ◽  
Ah Reum Noh ◽  
Kyeong-A. Kim ◽  
Muhammad Akram ◽  
Young-Jun Shin ◽  
...  
Keyword(s):  
Brain Damage ◽  
Mitochondrial Function ◽  
Ischemic Brain Damage ◽  
Ischemic Brain

Blockade of central histaminergic H2 receptors facilitates catecholaminergic metabolism and aggravates ischemic brain damage in the rat telencephalon

2003 ◽  
Vol 974 (1-2) ◽  
pp. 117-126 ◽  
Author(s):  
Ryu Otsuka ◽  
Naoto Adachi ◽  
Gen Hamami ◽  
Keyue Liu ◽  
Toshihiro Yorozuya ◽  
...  
Keyword(s):  
Brain Damage ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
H2 Receptors
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