Protein kinase C-β mediates neuronal activation of Na+/H+ exchanger-1 during glutamate excitotoxicity

Lee, Bo Kyung; Yoon, Jae Seok; Lee, Min Goo

doi:10.1016/j.cellsig.2013.12.011

Cited by 12 publications

(19 citation statements)

References 24 publications

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“…Previous studies have confirmed that the activation of PKC is the major factor in CIRI [5,8,[35][36][37][38]. As previously reported, hypoxia-induced BBB permeability changes occur via a Cellular Physiology and Biochemistry…”

Section: Discussionmentioning

confidence: 49%

Hydrogen Sulfide Decreases Blood-Brain Barrier Damage via Regulating Protein Kinase C and Tight Junction After Cardiac Arrest in Rats

Zhu

Feng

et al. 2018

Cell Physiol Biochem

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Background/Aims: Hydrogen sulfide (H₂S) can decrease blood-brain barrier (BBB) permeability after cardiac arrest (CA) and resuscitation; however, the underlying mechanisms are not understood clearly. Methods: We investigated the effects of inhalation of H₂S on CA and resuscitation in a rat model of CA. We used Evans blue to detect the integrity of BBB and Western blot to assess the activation of protein kinase c (PKC) isozymes and the expression of Claudin-5, Occludin, and ZO-1. Neurological deficit scales and the 14-days survival rate were measured. Results: We determined that inhalation of 40 p.p.m or 80 p.p.m H₂S significantly decreased brain water content and Evans blue leakage, ameliorated neurologic deficit scale and improved 14-days survival rate. H₂S inhibited the activation of PKC-α, β I, β II and δ, impelled the activation of PKC-ε, and increased the expression of Claudin-5, Occludin and ZO-1. Conclusions: H₂S improved the integrity of BBB, mitigated brain edema; improved neurological outcome and 14-days survival rate in rats after CA and resuscitation. The beneficial effects of H₂S may be associated with inhibiting the activation of PKC-α, β I, β II and δ, promoting the activation of PKC-ε, and increasing the expression of Claudin-5, Occludin and ZO-1.

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Section: Discussionmentioning

confidence: 49%

Hydrogen Sulfide Decreases Blood-Brain Barrier Damage via Regulating Protein Kinase C and Tight Junction After Cardiac Arrest in Rats

Zhu

Feng

et al. 2018

Cell Physiol Biochem

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“…ERK1/2, p38MAPKs, and JNK were isolated as described previously [ 16 ]. Cells were harvested in RIPA buffer (150 NaCl, 20 Tris-HCl, 1% NP-40, 1% Na-deoxycholate, 1 EDTA, and protease inhibitors at pH 7.4 [mM]) and homogenized, and nuclei and cell debris were removed by centrifugation at 10,000 ×g for 15 min at 4°C.…”

Section: Methodsmentioning

confidence: 99%

Allium cepa Extract and Quercetin Protect Neuronal Cells from Oxidative Stress via PKC‐ε Inactivation/ERK1/2 Activation

Lee

Jung

2016

Oxidative Medicine and Cellular Longevity

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Oxidative stress plays an important role in the pathophysiology of various neurologic disorders. Allium cepa extract (ACE) and their main flavonoid component quercetin (QCT) possess antioxidant activities and protect neurons from oxidative stress. We investigated the underlying molecular mechanisms, particularly those linked to the antioxidant effects of the ACE. Primary cortical neuronal cells derived from mouse embryos were preincubated with ACE or QCT for 30 min and exposed to L-buthionine sulfoximine for 4~24 h. We found that ACE and QCT significantly decreased neuronal death and the ROS increase induced by L-buthionine-S, R-sulfoximine (BSO) in a concentration-dependent manner. Furthermore, ACE and QCT activated extracellular signal-regulated kinase 1/2 (ERK1/2), leading to downregulation of protein kinase C-ε (PKC-ε) in BSO-stimulated neuronal cells. In addition, ACE and QCT decreased the phosphorylated levels of p38 mitogen-activated protein kinase. Our results provide new insight into the protective mechanism of ACE and QCT against oxidative stress in neuronal cells. The results suggest that the inactivation of PKC-ε induced by phosphorylating ERK1/2 is responsible for the neuroprotective effect of ACE and QCT against BSO-induced oxidative stress.

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“…CML cells constitutively express HO-1, and the disease-related oncoprotein BCR/ABL up-regulates expression of HO-1 in Ba/F3 cells. NHE1 is an important target protein implied in reversal of IM resistance in K562/IM cell lines and BCR-ABL-positive patient cells independent of p-gp protein stability (35).…”

Section: Discussionmentioning

confidence: 99%

Induction of Heme Oxygenase-1 by Na+-H+ Exchanger 1 Protein Plays a Crucial Role in Imatinib-resistant Chronic Myeloid Leukemia Cells

Fang

Wang

et al. 2015

Journal of Biological Chemistry

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Background:Resistance toward imatinib (IM) hinders the treatment of advanced stage chronic myeloid leukemia (CML). Results: Induction of HO-1 contributed to the survival of K562R cells and IM-insensitive CML patients' cells during IM exposure. Conclusion: HO-1 had anti-apoptotic effects on IM-resistant CML cells. Significance: Inducing HO-1 expression via the PKC-␤/p38-MAPK pathway may promote tumor resistance to oxidative stress.

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Protein kinase C-β mediates neuronal activation of Na+/H+ exchanger-1 during glutamate excitotoxicity

Cited by 12 publications

References 24 publications

Hydrogen Sulfide Decreases Blood-Brain Barrier Damage via Regulating Protein Kinase C and Tight Junction After Cardiac Arrest in Rats

Hydrogen Sulfide Decreases Blood-Brain Barrier Damage via Regulating Protein Kinase C and Tight Junction After Cardiac Arrest in Rats

Allium cepa Extract and Quercetin Protect Neuronal Cells from Oxidative Stress via PKC‐ε Inactivation/ERK1/2 Activation

Induction of Heme Oxygenase-1 by Na+-H+ Exchanger 1 Protein Plays a Crucial Role in Imatinib-resistant Chronic Myeloid Leukemia Cells

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