Effects of Apamin on MPP + -Induced Calcium Overload and Neurotoxicity by Targeting CaMKII/ERK/p65/STAT3 Signaling Pathways in Dopaminergic Neuronal Cells
Parkinson's disease (PD), a neurodegenerative disorder, is characterized by the loss of dopaminergic (DA) neurons. The pathogenesis of PD is associated with several factors including oxidative stress, inflammation, and mitochondrial dysfunction. Ca signaling plays a vital role in neuronal signa...
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Published in | International journal of molecular sciences Vol. 23; no. 23; p. 15255 |
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Language | English |
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Abstract | Parkinson's disease (PD), a neurodegenerative disorder, is characterized by the loss of dopaminergic (DA) neurons. The pathogenesis of PD is associated with several factors including oxidative stress, inflammation, and mitochondrial dysfunction. Ca
signaling plays a vital role in neuronal signaling and altered Ca
homeostasis has been implicated in many neuronal diseases including PD. Recently, we reported that apamin (APM), a selective antagonist of the small-conductivity Ca
-activated K
(SK) channel, suppresses neuroinflammatory response. However, the mechanism(s) underlying the vulnerability of DA neurons were not fully understood. In this study, we investigated whether APM affected 1-methyl-4-phenyl pyridinium (MPP
)-mediated neurotoxicity in SH-SY5Y cells and rat embryo primary mesencephalic neurons. We found that APM decreased Ca
overload arising from MPP
-induced neurotoxicity response through downregulating the level of CaMKII, phosphorylation of ERK, and translocation of nuclear factor NFκB/signal transducer and activator of transcription (STAT)3. Furthermore, we showed that the correlation of MPP
-mediated Ca
overload and ERK/NFκB/STAT3 in the neurotoxicity responses, and dopaminergic neuronal cells loss, was verified through inhibitors. Our findings showed that APM might prevent loss of DA neurons via inhibition of Ca
-overload-mediated signaling pathway and provide insights regarding the potential use of APM in treating neurodegenerative diseases. |
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AbstractList | Parkinson’s disease (PD), a neurodegenerative disorder, is characterized by the loss of dopaminergic (DA) neurons. The pathogenesis of PD is associated with several factors including oxidative stress, inflammation, and mitochondrial dysfunction. Ca2+ signaling plays a vital role in neuronal signaling and altered Ca2+ homeostasis has been implicated in many neuronal diseases including PD. Recently, we reported that apamin (APM), a selective antagonist of the small-conductivity Ca2+-activated K+ (SK) channel, suppresses neuroinflammatory response. However, the mechanism(s) underlying the vulnerability of DA neurons were not fully understood. In this study, we investigated whether APM affected 1-methyl-4-phenyl pyridinium (MPP+)-mediated neurotoxicity in SH-SY5Y cells and rat embryo primary mesencephalic neurons. We found that APM decreased Ca2+ overload arising from MPP+-induced neurotoxicity response through downregulating the level of CaMKII, phosphorylation of ERK, and translocation of nuclear factor NFκB/signal transducer and activator of transcription (STAT)3. Furthermore, we showed that the correlation of MPP+-mediated Ca2+ overload and ERK/NFκB/STAT3 in the neurotoxicity responses, and dopaminergic neuronal cells loss, was verified through inhibitors. Our findings showed that APM might prevent loss of DA neurons via inhibition of Ca2+-overload-mediated signaling pathway and provide insights regarding the potential use of APM in treating neurodegenerative diseases. Parkinson's disease (PD), a neurodegenerative disorder, is characterized by the loss of dopaminergic (DA) neurons. The pathogenesis of PD is associated with several factors including oxidative stress, inflammation, and mitochondrial dysfunction. Ca signaling plays a vital role in neuronal signaling and altered Ca homeostasis has been implicated in many neuronal diseases including PD. Recently, we reported that apamin (APM), a selective antagonist of the small-conductivity Ca -activated K (SK) channel, suppresses neuroinflammatory response. However, the mechanism(s) underlying the vulnerability of DA neurons were not fully understood. In this study, we investigated whether APM affected 1-methyl-4-phenyl pyridinium (MPP )-mediated neurotoxicity in SH-SY5Y cells and rat embryo primary mesencephalic neurons. We found that APM decreased Ca overload arising from MPP -induced neurotoxicity response through downregulating the level of CaMKII, phosphorylation of ERK, and translocation of nuclear factor NFκB/signal transducer and activator of transcription (STAT)3. Furthermore, we showed that the correlation of MPP -mediated Ca overload and ERK/NFκB/STAT3 in the neurotoxicity responses, and dopaminergic neuronal cells loss, was verified through inhibitors. Our findings showed that APM might prevent loss of DA neurons via inhibition of Ca -overload-mediated signaling pathway and provide insights regarding the potential use of APM in treating neurodegenerative diseases. Parkinson’s disease (PD), a neurodegenerative disorder, is characterized by the loss of dopaminergic (DA) neurons. The pathogenesis of PD is associated with several factors including oxidative stress, inflammation, and mitochondrial dysfunction. Ca 2+ signaling plays a vital role in neuronal signaling and altered Ca 2+ homeostasis has been implicated in many neuronal diseases including PD. Recently, we reported that apamin (APM), a selective antagonist of the small-conductivity Ca 2+ -activated K + (SK) channel, suppresses neuroinflammatory response. However, the mechanism(s) underlying the vulnerability of DA neurons were not fully understood. In this study, we investigated whether APM affected 1-methyl-4-phenyl pyridinium (MPP + )-mediated neurotoxicity in SH-SY5Y cells and rat embryo primary mesencephalic neurons. We found that APM decreased Ca 2+ overload arising from MPP + -induced neurotoxicity response through downregulating the level of CaMKII, phosphorylation of ERK, and translocation of nuclear factor NFκB/signal transducer and activator of transcription (STAT)3. Furthermore, we showed that the correlation of MPP + -mediated Ca 2+ overload and ERK/NFκB/STAT3 in the neurotoxicity responses, and dopaminergic neuronal cells loss, was verified through inhibitors. Our findings showed that APM might prevent loss of DA neurons via inhibition of Ca 2+ -overload-mediated signaling pathway and provide insights regarding the potential use of APM in treating neurodegenerative diseases. |
Author | Jang, Kyung Mi Park, Kwan-Kyu Park, Jihyun |
AuthorAffiliation | 1 Department of Pathology, College of Medicine, Catholic University of Daegu, Daegu 42472, Republic of Korea 2 Department of Pediatrics, College of Medicine, Yeungnam University, Daegu 42415, Republic of Korea |
AuthorAffiliation_xml | – name: 1 Department of Pathology, College of Medicine, Catholic University of Daegu, Daegu 42472, Republic of Korea – name: 2 Department of Pediatrics, College of Medicine, Yeungnam University, Daegu 42415, Republic of Korea |
Author_xml | – sequence: 1 givenname: Jihyun surname: Park fullname: Park, Jihyun organization: Department of Pathology, College of Medicine, Catholic University of Daegu, Daegu 42472, Republic of Korea – sequence: 2 givenname: Kyung Mi orcidid: 0000-0002-2226-9268 surname: Jang fullname: Jang, Kyung Mi organization: Department of Pediatrics, College of Medicine, Yeungnam University, Daegu 42415, Republic of Korea – sequence: 3 givenname: Kwan-Kyu orcidid: 0000-0002-5317-750X surname: Park fullname: Park, Kwan-Kyu organization: Department of Pathology, College of Medicine, Catholic University of Daegu, Daegu 42472, Republic of Korea |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/36499581$$D View this record in MEDLINE/PubMed |
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Keywords | apoptosis oxidant stress SK channel Parkinson’s disease apamin ROS |
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Snippet | Parkinson's disease (PD), a neurodegenerative disorder, is characterized by the loss of dopaminergic (DA) neurons. The pathogenesis of PD is associated with... Parkinson’s disease (PD), a neurodegenerative disorder, is characterized by the loss of dopaminergic (DA) neurons. The pathogenesis of PD is associated with... |
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SubjectTerms | 1-Methyl-4-phenylpyridinium - toxicity Animals apamin Apamin - pharmacology Apoptosis Ca2+/calmodulin-dependent protein kinase II Calcium (mitochondrial) Calcium - metabolism Calcium antagonists Calcium homeostasis Calcium ions Calcium signalling Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism Cell Line, Tumor Cytotoxicity Dopamine receptors Dopaminergic Neurons - metabolism Extracellular signal-regulated kinase Homeostasis Humans Inflammation Mitochondria Morphology MPP Neuroblastoma - metabolism Neurons Neuroprotective Agents - pharmacology Neurotoxicity Neurotoxicity Syndromes - pathology NF-kappa B - metabolism NF-κB protein Overloading oxidant stress Oxidative Stress Parkinson Disease - metabolism Parkinson's disease Pathogenesis Phosphorylation Potassium channels (calcium-gated) Proteins Rats ROS Signal Transduction SK channel Stat3 protein |
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Title | Effects of Apamin on MPP + -Induced Calcium Overload and Neurotoxicity by Targeting CaMKII/ERK/p65/STAT3 Signaling Pathways in Dopaminergic Neuronal Cells |
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