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Inhibitor 1 of Protein Phosphatase 1 Regulates Ca2+Calmodulin-Dependent Protein Kinase II to Alleviate Oxidative Stress in Hypoxia-Reoxygenation Injury of Cardiomyocytes
Joint Authors
Meng, Guoliang
Luo, Huiqin
Song, Shu
Chen, Yun
Xu, Mengting
Sun, Linlin
Zhang, Wei
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2019, Issue 2019 (31 Dec. 2019), pp.1-19, 19 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2019-12-07
Country of Publication
Egypt
No. of Pages
19
Main Subjects
Abstract EN
Ca2+/calmodulin-dependent protein kinase II (CaMKII), regulated by inhibitor 1 of protein phosphatase 1 (I1PP1), is vital for maintaining cardiovascular homeostasis.
However, the role and mechanism of I1PP1 against hypoxia-reoxygenation (H/R) injury in cardiomyocytes remain a question.
In our study, after I1PP1 overexpression by adenovirus infection in the neonatal cardiomyocytes followed by hypoxia for 4 h and reoxygenation for 12 h, the CaMKIIδ alternative splicing subtype, ATP content, and lactate dehydrogenase (LDH) release were determined.
CaMKII activity was evaluated by phosphoprotein phosphorylation at Thr17 (p-PLB Thr17), CaMKII phosphorylation (p-CaMKII), and CaMKII oxidation (ox-CaMKII).
Reactive oxygen species (ROS), mitochondrial membrane potential, dynamin-related protein 1 (DRP1), and optic atrophy 1 (OPA1) expressions were assessed.
Our study verified that I1PP1 overexpression attenuated the CaMKIIδ alternative splicing disorder; suppressed PLB phosphorylation at Thr17, p-CaMKII, and ox-CaMKII; decreased cell LDH release; increased ATP content; attenuated ROS production; increased mitochondrial membrane potential; and decreased DRP1 expression but increased OPA1 expression in the cardiomyocytes after H/R.
Contrarily, CaMKIIδ alternative splicing disorder, LDH release, ATP reduction, and ROS accumulation were aggravated after H/R injury with the I1PP1 knockdown.
Collectively, I1PP1 overexpression corrected disorders of CaMKIIδ alternative splicing, inhibited CaMKII phosphorylation, repressed CaMKII oxidation, suppressed ROS production, and attenuated cardiomyocyte H/R injury.
American Psychological Association (APA)
Luo, Huiqin& Song, Shu& Chen, Yun& Xu, Mengting& Sun, Linlin& Meng, Guoliang…[et al.]. 2019. Inhibitor 1 of Protein Phosphatase 1 Regulates Ca2+Calmodulin-Dependent Protein Kinase II to Alleviate Oxidative Stress in Hypoxia-Reoxygenation Injury of Cardiomyocytes. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-19.
https://search.emarefa.net/detail/BIM-1202546
Modern Language Association (MLA)
Luo, Huiqin…[et al.]. Inhibitor 1 of Protein Phosphatase 1 Regulates Ca2+Calmodulin-Dependent Protein Kinase II to Alleviate Oxidative Stress in Hypoxia-Reoxygenation Injury of Cardiomyocytes. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-19.
https://search.emarefa.net/detail/BIM-1202546
American Medical Association (AMA)
Luo, Huiqin& Song, Shu& Chen, Yun& Xu, Mengting& Sun, Linlin& Meng, Guoliang…[et al.]. Inhibitor 1 of Protein Phosphatase 1 Regulates Ca2+Calmodulin-Dependent Protein Kinase II to Alleviate Oxidative Stress in Hypoxia-Reoxygenation Injury of Cardiomyocytes. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-19.
https://search.emarefa.net/detail/BIM-1202546
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1202546