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

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...

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Veröffentlicht in:Neural plasticity. - 1998. - 2015(2015) vom: 01., Seite 374520
1. Verfasser: Song, Juhyun (VerfasserIn)
Weitere Verfasser: Cheon, So Yeong, Lee, Won Taek, Park, Kyung Ah, Lee, Jong Eun
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2015
Zugriff auf das übergeordnete Werk:Neural plasticity
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Apoptosis Regulatory Proteins Brain-Derived Neurotrophic Factor Disks Large Homolog 4 Protein Dlg4 protein, mouse Isoquinolines Membrane Proteins Microtubule-Associated Proteins Mtap2 protein, mouse mehr... Protein Kinase Inhibitors Sulfonamides Cyclic AMP-Dependent Protein Kinases EC 2.7.11.11 Guanylate Kinases EC 2.7.4.8 N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide M876330O56
Beschreibung
Zusammenfassung: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
Beschreibung:Date Completed 19.07.2016
Date Revised 13.11.2018
published: Print-Electronic
Citation Status MEDLINE
ISSN:1687-5443
DOI:10.1155/2015/374520