Intermittent-hypoxia induced autophagy attenuates contractile dysfunction and myocardial injury in rat heart

Maeda, Hideyuki; Nagai, Hisashi; Takemura, Genzou; Shintani-Ishida, Kaori; Komatsu, Masaaki; Ogura, Sayoko; Aki, Toshihiko; Shirai, Mikiayasu; Kuwahira, Ichiro; Yoshida, Ken

doi:10.1016/j.bbadis.2013.02.014

Cited by 60 publications

(48 citation statements)

References 32 publications

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“…By contrast, in a minipig LAD model, the immunosuppressant tacrolimus, or FK-506 or fujimycin, a 23-membered macrolide lactone, was shown to limit infarct by suppressing the inflammatory response through down-regulation of the Akt signaling pathways [60], but the same substance also upregulates HO-1, which is at odds with our observations. Interestingly, in an OSA model where IH is not protective, Akt Ser 473 phosphorylation was found to be decreased [61], in agreement with present data. Akt activation may also provide protection via increased eNOS and augmented NO stores.…”

Section: Ih-induced Signaling Pathwayssupporting

confidence: 81%

Impact of phosphatidylinositide 3-kinase signaling pathway on the cardioprotection induced by intermittent hypoxia

et al. 2014

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Section: Ih-induced Signaling Pathwayssupporting

confidence: 81%

Impact of phosphatidylinositide 3-kinase signaling pathway on the cardioprotection induced by intermittent hypoxia

et al. 2014

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“…These results showed that fucoidan suppressed high hypoxia-induced cardiomyoblast cells oxidative stress which is indicated by inhibiting LDH and CK activities. Although the exact etiology is still unknown, extensive studies for the last several decades have shown that hypoxiainduced cardiac myocyte loss plays a major part in patients with many kinds of heart diseases (Maeda et al, 2013). In recent years, more and more attention has been focused on researching the chemical substance and nature compounds (A) (B) Figure 3.…”

Section: Discussionmentioning

confidence: 99%

Cardioprotective effects of fucoidan against hypoxia-induced apoptosis in H9c2 cardiomyoblast cells

Zhang

Xie

et al. 2015

Pharmaceutical Biology

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Context: Cardiomyocyte apoptosis plays a critical role in the progress of heart diseases. Fucoidan, a complex-sulfated polysaccharide, has been reported to possess potential cardioprotective efficacy in vivo. Objective: The present study determines whether fucoidan could provide cardioprotection on hypoxia-induced cardiomyocyte apoptosis. Materials and methods: H9c2 cardiomyoblast cells were incubated with various concentrations (15, 30, and 60 lg/ml) of fucoidan in a humidified incubator at 37 C with 95% O 2 and 5% CO 2 . After 6 h, hypoxia was processed and the cardioprotective effects of fucoidan were evaluated by applying MTT, ELISA, Hoechst 33258 nucleus staining, and western blot.Results: Following a 6 h exposure of H9c2 to hypoxic condition, significant reduction was found in cell survival (0.57-fold) and superoxide dismutase (SOD) activity (0.56-fold), which were associated with the increase of malondialdehyde (MDA) level (2.58-fold), creatine phosphokinase (CK, 3.57-fold), and lactate dehydrogenase (LDH) activities (2.39-fold). Moreover, hypoxiainduced apoptosis was confirmed by Hoechst 33258 nuclear staining, and these changes were accompanied by the increase of Bcl-2 (1.27-fold) and Bax expression (2.6-fold). However, preincubation of the cells with fucoidan prior to hypoxia exposure elevated the cell viability (30 lg/ml, 1.18-fold; 60 lg/ml, 1.32-fold) and SOD activity (30 lg/ml, 1.12-fold; 60 lg/ml, 1.25-fold), but decreased the MDA level (30 lg/ml, 0.70-fold; 60 lg/ml, 0.80-fold), CK (30 lg/ml, 0.69-fold; 60 lg/ml, 0.76-fold), and LDH (30 lg/ml, 0.67-fold; 60 lg/ml, 0.86-fold) leakages. Hoechst 33258 nuclear staining observations demonstrated the same protective effect of fucoidan on hypoxia-induced myocardial injury. Also, cardioprotective effects of fucoidan were reflected by increasing Bcl-2 (60 lg/ml, 1.84-fold), as well as decreasing Bax (60 lg/ml, 0.6-fold). Conclusion: Fucoidan had protective effect against hypoxia-induced cardiomyocytes apoptosis, and the mechanism might involve protections of the cell from oxidative injury.

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“…Superthin slices (70 nm; UC07; Leica, Wetzler, Germany) were well prepared, and stained with uranyl acetate and lead citrate. 21 Finally, specimens were observed by transmission electron microscopy (JEM-1200EX; JEOL, Tokyo, Japan).…”

Section: Transmission Electron Microscopymentioning

confidence: 99%

Rosuvastatin Alleviates Type 2 Diabetic Atrial Structural and Calcium Channel Remodeling

Pan

Li²,

Wang³

et al. 2016

Journal of Cardiovascular Pharmacology

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Recent evidence has indicated that type 2 diabetes mellitus is related to an increased risk of atrial arrhythmias, which might result from atrial structural and electrical remodeling. Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase (statins), known as lipid-lowering agents, have been shown to exert antiarrhythmic effects both in experimental models and in humans. In this study, we postulate that atrial structural and calcium channel remodeling may occur in streptozotocin-induced type 2 diabetic rats and can be alleviated by rosuvastatin (RSV) therapy. We randomly divided Wistar rats into control, untreated diabetic, RSV-treated control, and RSV-treated diabetic animals. After treatment with RSV for 4 weeks, rats were assessed by metabolic tests, histopathology, and transmission electron microscopy. The expression of Cav1.2, Cav3.1, and Cav3.2 in atrial tissues was detected by real-time reverse transcriptase polymerase chain reaction and Western blot, and inward calcium currents (l(Ca-L) and l(Ca-T)) were recorded in isolated atrial myocytes using patch-clamp techniques. Compared with controls, diabetic rats displayed severe metabolic disorders and a disorganized cellular ultrastructure. In diabetic rats, the expression of Cav1.2 mRNA and protein was significantly decreased, whereas that of Cav3.1 was significantly increased. Long-term RSV treatment partially relieved some pathological changes in diabetic rats. However, Cav3.2 mRNA and protein remained unchanged in control and diabetic groups and was unaffected by RSV. Diabetic atrial myocytes showed significantly reduced L-type but increased T-type, Ca (2+) currents, and this effect was significantly reversed by RSV. In conclusion, long-term RSV therapy can alleviate structural and calcium channel remodeling in the type 2 diabetic rat atrium.

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Intermittent-hypoxia induced autophagy attenuates contractile dysfunction and myocardial injury in rat heart

Cited by 60 publications

References 32 publications

Impact of phosphatidylinositide 3-kinase signaling pathway on the cardioprotection induced by intermittent hypoxia

Impact of phosphatidylinositide 3-kinase signaling pathway on the cardioprotection induced by intermittent hypoxia

Cardioprotective effects of fucoidan against hypoxia-induced apoptosis in H9c2 cardiomyoblast cells

Rosuvastatin Alleviates Type 2 Diabetic Atrial Structural and Calcium Channel Remodeling

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