Prokineticin 2 (PK2) Rescues Cardiomyocytes from High GlucoseHigh Palmitic Acid-Induced Damage by Regulating the AKTGSK3β Pathway In Vitro
Joint Authors
Yu, Wei
Zha, Wenliang
Yang, Zhen
Wu, Yin
Wang, Linge
Qiu, Peng
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-17, 17 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2020-05-18
Country of Publication
Egypt
No. of Pages
17
Main Subjects
Abstract EN
Prokineticin 2 (PK2) is a small 8 kDa protein that participates in many physiological processes, such as angiogenesis, inflammation, and neurogenesis.
This experiment investigated the effect of PK2 on high glucose/high palmitic acid-induced oxidative stress, apoptosis, and autophagy in cardiomyocytes and the AKT/GSK3β signalling pathway.
H9c2 cells were exposed to normal and high concentrations (33 mM) of glucose and palmitic acid (150 μM) with or without PK2 (10 nM) for 48 h.
Reactive oxygen species were detected using the fluorescent probes DCFH-DA and DHE.
Changes in apoptosis were assessed using flow cytometry, and autophagosomes were detected using Ad-GFP-LC3.
Apoptotic proteins, such as Cleaved Caspase3, Bax, and Bcl-2; autophagy proteins, including Beclin-1 and LC3B; and PK2/PKR/AKT/GSK3β signals were evaluated using western blotting.
Cardiomyocytes exposed to high glucose/high palmitic acid exhibited increases in intracellular ROS, apoptosis, and autophagosomes, and these increases were robustly prevented by PK2.
In addition, high glucose/high palmitic acid remarkably suppressed PK2, PKR1, and PKR2 expression and p-AKT/AKT and p-GSK3β/GSK3β ratios, and these effects were significantly prevented by PK2.
Moreover, an AKT1/2 kinase inhibitor (AKT inhibitor, 10 μM) blocked the effects of PK2 on the changes in cardiomyocyte exposure to high glucose/high palmitic acid.
These results suggest that PK2 attenuates high glucose/high palmitic acid-induced cardiomyocyte apoptosis by inhibiting oxidative stress and autophagosome accumulation and that this protective effect is most likely mediated by the AKT-related signalling pathway.
American Psychological Association (APA)
Yang, Zhen& Wu, Yin& Wang, Linge& Qiu, Peng& Zha, Wenliang& Yu, Wei. 2020. Prokineticin 2 (PK2) Rescues Cardiomyocytes from High GlucoseHigh Palmitic Acid-Induced Damage by Regulating the AKTGSK3β Pathway In Vitro. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-17.
https://search.emarefa.net/detail/BIM-1204181
Modern Language Association (MLA)
Yang, Zhen…[et al.]. Prokineticin 2 (PK2) Rescues Cardiomyocytes from High GlucoseHigh Palmitic Acid-Induced Damage by Regulating the AKTGSK3β Pathway In Vitro. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-17.
https://search.emarefa.net/detail/BIM-1204181
American Medical Association (AMA)
Yang, Zhen& Wu, Yin& Wang, Linge& Qiu, Peng& Zha, Wenliang& Yu, Wei. Prokineticin 2 (PK2) Rescues Cardiomyocytes from High GlucoseHigh Palmitic Acid-Induced Damage by Regulating the AKTGSK3β Pathway In Vitro. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-17.
https://search.emarefa.net/detail/BIM-1204181
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1204181