C-Phycocyanin Ameliorates Mitochondrial Fission and Fusion Dynamics in Ischemic Cardiomyocyte Damage

Abstract

Mitochondrial dysfunction is a predominant risk factor in ischemic heart disease, in which the imbalance of mitochondrial fusion and fission deteriorates mitochondrial function and might lead to cardiomyocyte death. C-phycocyanin (C-pc), an active component from blue-green algae, such as Spirulina platensis , has been reported to have anti-apoptosis and anti-oxidation functions. In this study, the effects of C-pc on mitochondrial dynamics of cardiomyocytes was examined using an oxygen–glucose deprivation/reoxygenation (OGD/R) model in H9c2 cells, an in vitro model to study the ischemia in the heart. Cell viability assay showed that C-pc dose-dependently reduced OGD/R-induced cell death. Intracellular reactive oxygen species production induced by OGD/R was decreased in C-pc-treated groups in a dose-dependent manner as well. H9c2 cells subjected to OGD/R showed excessive mitochondrial fission and diminished mitochondrial fusion. C-pc treatment significantly ameliorated unbalanced mitochondrial dynamics induced by OGD/R and regulated mitochondrial remodeling through inhibiting mitochondrial fission while promoting fusion. The enhanced expressions of dynamin 1-like protein and mitochondrial fission 1 protein induced by OGD/R were suppressed by C-pc, while the subdued expressions of mitochondrial fusion proteins mitofusins 1 and 2 and optic atrophy 1 induced by OGD/R increased in C-pc-treated groups. Triple immunofluorescence staining revealed that C-pc treatment reduced the recruitment of dynamin 1-like protein from cytoplasm to mitochondrial membranes. Furthermore, C-pc protected H9c2 cells against OGD/R-induced cytochrome c/apoptotic protease activating factor-1 intrinsic apoptosis and suppressed the phosphorylations of extracellular signal-regulated kinase and c-Jun N-terminal kinase. These results suggest that C-pc protects cardiomyocytes from ischemic damage by affecting mitochondrial fission and fusion dynamics and reducing apoptosis and, thus, may be of potential as a prophylactic or therapeutic agent for ischemic heart disease.

[Retracted] Natural Antioxidants Improve the Vulnerability of Cardiomyocytes and Vascular Endothelial Cells under Stress Conditions: A Focus on Mitochondrial Quality Control

“…The mammalian mitochondrial genome has 37 genes, 13 of which encode polypeptide subunits of enzyme complexes of the oxidative phosphorylation system, which provides more than 95% of the myocardial energy requirement for adenosine triphosphate (ATP) production [ 16 , 17 ]. Mitochondria are the main organelles that mediate the energy production and apoptosis of cardiomyocytes [ 18 , 19 ]. Because of the high energy requirement of myocardial cells, MQC is very important in these cells.…”

High‐intensity interval training along with spirulina algae consumption and caloric restriction ameliorated the Nrf1/Tfam/Mgmt and ATP5A1 pathway in the heart tissue of obese rats

“…On the other hand, our results showed that caloric restriction enhanced the relative expression of Nrf1/Tfam/Mgmt and ATP5A1 network in the heart tissue. In this regard, studies have shown that resistance training and a caloric restriction increased mitochondrial fission protein (Opa1 and Mfn1) and PGC-1α expression in the skeletal muscle of rats (Gao et al, 2019).…”

Sex Hormone Regulation of Proteins Modulating Mitochondrial Metabolism, Dynamics and Inter-Organellar Cross Talk in Cardiovascular Disease

“…Therefore, further studies are necessary to better understand how signaling via both estrogen and testosterone influence cardiac apoptosis in CVD. Necrosis and pyroptosis are inflammatory cell death pathways regulated via caspase enzyme activity, which is induced when irreversible damage occurs in the tissues ( Bergsbaken et al, 2009 ; Gao et al, 2019 ; Zhaolin et al, 2019 ). These pathways, more specifically, are initiated when the MPTP is damaged or uncontrolled in mitochondrial fission, as seen in CVD ( Song et al, 2015 ; Amgalan et al, 2020 ).…”