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PKA Inhibitor H89 (N-[2-p-bromocinnamylamino-ethyl]-5-isoquinolinesulfonamide) Attenuates Synaptic Dysfunction and Neuronal Cell Death following Ischemic Injury

Authors
 Juhyun Song  ;  So Yeong Cheon  ;  Won Taek Lee  ;  Kyung Ah Park  ;  Jong Eun Lee 
Citation
 NEURAL PLASTICITY, Vol.2015 : 374520, 2015 
Journal Title
 NEURAL PLASTICITY 
ISSN
 2090-5904 
Issue Date
2015
MeSH
Animals ; Apoptosis Regulatory Proteins/genetics ; Apoptosis Regulatory Proteins/metabolism ; Brain Ischemia/drug therapy* ; Brain Ischemia/pathology* ; Brain-Derived Neurotrophic Factor/biosynthesis ; Cell Death/drug effects* ; Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors* ; Disks Large Homolog 4 Protein ; Guanylate Kinases/genetics ; Hypoxia, Brain/pathology ; Infarction, Middle Cerebral Artery/drug therapy ; Infarction, Middle Cerebral Artery/pathology ; Isoquinolines/therapeutic use* ; Male ; Membrane Proteins/genetics ; Mice ; Mice, Inbred C57BL ; Microtubule-Associated Proteins/genetics ; Neurons/drug effects* ; Neurons/ultrastructure ; Protein Kinase Inhibitors/therapeutic use* ; Reperfusion Injury/drug therapy ; Reperfusion Injury/pathology ; Sulfonamides/therapeutic use* ; Synapses/drug effects* ; Synapses/ultrastructure
Abstract
The cyclic AMP-dependent protein kinase (PKA), which activates prosurvival signaling proteins, has been implicated in the expression of long-term potentiation and hippocampal long-term memory. It has come to light that H89 commonly known as the PKA inhibitor have diverse roles in the nervous system that are unrelated to its role as a PKA inhibitor. We have investigated the role of H89 in ischemic and reperfusion injury. First, we examined the expression of postsynaptic density protein 95 (PSD95), microtubule-associated protein 2 (MAP2), and synaptophysin in mouse brain after middle cerebral artery occlusion injury. Next, we examined the role of H89 pretreatment on the expression of brain-derived neurotrophic factor (BDNF), PSD95, MAP2, and the apoptosis regulators Bcl2 and cleaved caspase-3 in cultured neuroblastoma cells exposed to hypoxia and reperfusion injury. In addition, we investigated the alteration of AKT activation in H89 pretreated neuroblastoma cells under hypoxia and reperfusion injury. The data suggest that H89 may contribute to brain recovery after ischemic stroke by regulating neuronal death and proteins related to synaptic plasticity.
Files in This Item:
T201502263.pdf Download
DOI
10.1155/2015/374520
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Anatomy (해부학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
Yonsei Authors
Park, Kyung Ah(박경아)
Song, Ju Hyun(송주현)
Lee, Won Taek(이원택) ORCID logo https://orcid.org/0000-0001-7348-9562
Lee, Jong Eun(이종은) ORCID logo https://orcid.org/0000-0001-6203-7413
Cheon, So Yeong(전소영)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/140588
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