PT363 A Novel Cytokine, Interleukin-27, Protects Rat Cardiomyocytes Against Ischemia-Reperfusion Injury

Global Heart ◽  
2014 ◽  
Vol 9 (1) ◽  
pp. e239-e240
Author(s):  
Ming-Chieh Ma ◽  
Yu-Tzu Huang
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Rat Cardiomyocytes ◽  
Interleukin 27

scholarly journals Follistatin-Like 1 Attenuates Ischemia/Reperfusion Injury in Cardiomyocytes via Regulation of Autophagy

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Weijun Yang ◽  
Qunjun Duan ◽  
Xian Zhu ◽  
Kaiyu Tao ◽  
Aiqiang Dong
Keyword(s):  
Cell Viability ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Annexin V ◽  
Protective Role ◽  
Autophagic Flux ◽  
Rat Cardiomyocytes ◽  
Hypoxia Ischemia ◽  
Myocardial Ischemia Reperfusion

Background. The cardioprotective effect of FSTL1 has been extensively studied in recent years, but its role in myocardial ischemia/reperfusion injury (IRI) is unclear. In this study, we investigated the effect of FSTL1 pretreatment on myocardial IRI as well as the possible involvement of autophagic pathways in its effects. Methods. The effects of FSTL1 on the viability and apoptosis of rat cardiomyocytes were investigated after exposure of cardiomyocytes to hypoxia/ischemia by using the CCK-8 assay and Annexin V/PI staining. Further, western blot analysis was used to detect the effects of FSTL1 pretreatment on autophagy-associated proteins, and confocal microscopy was used to observe autophagic flux. To confirm the role of autophagy, the cells were treated with the autophagy promoter rapamycin or the autophagy inhibitor 3-methyladenine, and cell viability and apoptosis during IRI were observed. These effects were also observed after treatment with rapamycin or 3-methyladenine followed by FSTL1 administration and IRI. Results. FSTL1 pretreatment significantly increased viability and reduced apoptosis in cardiomyocytes exposed to hypoxia/ischemia conditions. Further, FSTL1 pretreatment affected the levels of the autophagy-related proteins and enhanced autophagic flux during IRI. In addition, cell viability was enhanced and apoptosis was decreased by rapamycin treatment, while these effects were reversed by 3-MA treatment. However, when the myocardial cells were pretreated with rapamycin or 3-methyladenine, there was no significant change in their viability or apoptosis with FSTL1 treatment during IRI. Conclusions. FSTL1 plays a protective role in myocardial IRI by regulating autophagy.

Abstract 354: Prostaglandin D 2 -F Type Prostanoid Receptor Signaling Is a Novel Cardiomyocyte Survival Pathway

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Yoshinori Katsumata ◽  
Motoaki Sano ◽  
Tomohiro Matsuhashi ◽  
Atsushi Anzai ◽  
Cardex Yan ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Expression Profiles ◽  
Ischemia Reperfusion ◽  
Cardioprotective Effect ◽  
Neonatal Rat ◽  
Th2 Cells ◽  
Dependent Manner ◽  
Rat Cardiomyocytes ◽  
Fp Receptor

Background: Lipocalin-type prostaglandin D synthase (L-PGDS) is abundantly expressed on cardiomyocytes. We recently demonstrated that dexamethasone stimulates PGD 2 -dominated activation of prostanoid biosynthesis, thereby protecting hearts against ischemia/reperfusion injury. Here, we examined the downstream signaling responsible for cardioprotection mediated through PGD 2 -dominated activation. Methods and Results: (1) In cultured neonatal rat cardiomyocytes, PGD 2 strongly activates ERK in a dose-dependent manner, although canonical PGD 2 receptors, including DP (PGD 2 receptor) and CRTH2 (chemoattractant receptor-homologous molecule expressed on Th2 cells) receptors, are hardly expressed on cardiomyocytes. (2) Interestingly, PGD 2 bounds to FP receptor (the canonical PGF 2 α receptor) with an affinity comparable to that for the DP receptor, and the FP receptor is abundantly expressed on cardiomyocytes. (3) PGD 2 -induced ERK activation is completely blocked by FP antagonist or siRNA-mediated knockdown of the FP, but not by DP and CRTH2 antagonist and siRNA-mediated knockdown of DP and CRTH2. (4) PGD 2 activates ERK in Langendorff perfused DP-knock out (KO) and CRTH2-KO mice hearts to comparable levels as those observed for wild-type hearts, while cannot activate it in FP-KO hearts. (5) Consistently, the cardioprotective effect of PGD 2 -dominated activation by dexamethasone was blunted in FP KO hearts. (6) Furtermore, genomewide gene expression profiles by microarray analysis and quantitative real-time RT-PCR analysis identified that Nrf-2 was the downstream target of L-PGDS-mediated PGD 2 biosynthesis. (7) In cultured cardiomyocytes, FP agonist stimulated Nrf2 nuclear translocation and consequently induced Nrf2-target genes expression in an ERK-dependent manner. (8) Finally, The cardioprotective effect by dexamethasone was completely abolished in Nrf-2 KO hearts. Conclusion: FP serves as a functionally relevant PGD 2 receptor in the hearts and PGD 2 -FP signaling plays a substantial role in the improvement of functional recovery after ischemia-reperfusion injury in the heart. Nrf-2 is a major effector molecule responsible for the cardioprotecton elicited by L-PGDS-derived PGD 2 .

Resveratrol Nanoparticle Complex: Potential Therapeutic Applications in Myocardial Ischemia Reperfusion Injury

2020 ◽  
Vol 16 (3) ◽  
pp. 382-389
Author(s):  
Hong Zhou ◽  
Yungang Shan ◽  
Fei Tong ◽  
Yi Zhang ◽  
Jie Tang ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Half Life ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Proton Nuclear Magnetic Resonance ◽  
Release Time ◽  
Rat Cardiomyocytes ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Resveratrol (RES) is a natural non-flavonoid polyphenol with cardioprotective activities, antioxidant, antiplatelet, and antiinflammatory. However, its low aqueous solubility, chemical stability, and oral bioavailability, as well as a short circulation half-life greatly limit its clinical applications. To overcome these limitations of RES, we synthesized a methoxy poly(ethylene glycol)-b-oligomerization(D, L-Leucine) (mPEG-b-O(D, L-Leu)) nanoparticle (NP) as the carrier of RES and evaluated the myocardial-protective effectiveness of this RES/NP complex in rat myocardial ischemia-reperfusion injury models. We gauged the characterization of the NP through proton nuclear magnetic resonance spectroscopy, gel permeation chromatography, transmission electron microscope, and Fourier transform infrared spectroscopy and then loaded RES on the nanocarrier by hydrophobic interactions under physiological pH to extend the release time of RES and prolong its circulation half-life. Subsequently, we used rat cardiomyocytes (H9C2 cells) and rat MI/RI model to investigate the relationship between drug composition and myocardial preservation properties. It was found that RES was encapsulated quickly and efficiently, and displayed an effectual loading-capacity and in vitro sustained-release. Anti-MI/RI effect of the RES/NP complex was found satisfactory in rat models in vivo using free RES as the control. This study suggested that NP may prove to be a potent nanocarrier to augment the pharmacotherapy of RES against MI/RI.

scholarly journals RRM2 Improves Cardiomyocyte Proliferation after Myocardial Ischemia Reperfusion Injury through the Hippo-YAP Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Huamin Yu ◽  
Haiyan Tang ◽  
Chaochao Deng ◽  
Qing Lin ◽  
Peng Yu ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Neonatal Rat ◽  
Cell Counting ◽  
Cardiomyocyte Proliferation ◽  
Rat Cardiomyocytes ◽  
Qrt Pcr ◽  
Myocardial Ischemia Reperfusion ◽  
Deoxyribonucleoside Triphosphate

Objective. Ribonucleotide reductase M2 (RRM2) as an enzyme that catalyzes the deoxyreduction of nucleosides to deoxyribonucleoside triphosphate (dNTP) has been extensively studied, and it plays a crucial role in regulating cell proliferation. However, its role in ischemia-reperfusion injury (I/RI) is still unclear. Methods. SD rats were used as the research object to detect the expression of RRM2 in the myocardium by constructing an I/RI model. At the same time, primary SD neonatal rat cardiomyocytes were extracted, and hypoxia/reoxygenation (H/R) treatment simulated the I/RI model. Using transfection technology to overexpress RRM2 in cardiomyocytes, quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) was used to detect the expression of RRM2, Cell Counting Kit-8 (CCK-8) assay was used to detect cell viability, and immunofluorescence staining was used to detect Ki67 and EdU-positive cells. Western blot (WB) technology was used to detect YAP and its phosphorylation expression. Results. qRT-PCR results indicated that the expression of RRM2 was inhibited in the model group, and cardiomyocytes overexpressing RRM2 can obviously promote the proliferation of primary cardiomyocytes and improve the damage of cardiac structure and function caused by I/R. At the same time, RRM2 can promote the increase of YAP protein expression and the increase of Cyclin D1 mRNA expression. Conclusion. RRM2 expression was downregulated in myocardial tissue with I/R. After overexpression of RRM2, cardiomyocyte proliferation was upregulated and the Hippo-YAP signaling pathway was activated.

Abstract 257: Berbamine Postconditioning Protects the Heart From Ischemia/Reperfusion Injury Through the Regulation of Autophagy During Reperfusion

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Yanjun Zheng ◽  
Xuxia Li ◽  
Jinxi Wang ◽  
Jiliang Tan ◽  
Caimei Zhang ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Signaling Pathway ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Modern Society ◽  
Akt Signaling ◽  
Beclin 1 ◽  
Akt Signaling Pathway ◽  
Cardiovascular Research ◽  
Rat Cardiomyocytes

Myocardial infarction resulting from coronary atherosclerosis is the leading cause of death in modern society. Reperfusion is an essential treatment to salvage ischemia myocardium from necrosis, while it also leads to additional damage. Therefore, exploring effective medicines to protect the heart from post-ischemic injury is one of the major objectives of cardiovascular research. Berbamine, a nature compound of bisbenzylisochinoline alkaloids from Barberry, protects the heart from ischemia/reperfusion (I/R) injury when given before I/R, but it is unknown whether it has cardioprotective effects when given at the onset of reperfusion (postconditioning, PoC), a protocol with more clinical impact. Therefore, the present study was designed to determine whether berbamine PoC (BMPoC) is able to protect the heart from reperfusion injury by using perfused I/R rat hearts and simulated I/R cardiomyocytes. We found that BMPoC added during the first 5-min of reperfusion concentration-dependently improved post-ischemic myocardial function and limited infarcted area. A similar protection was observed in isolated rat cardiomyocytes characterized by the attenuation of I/R-induced depression of cell contraction and loss of mitochondrial membrane potential. Moreover, autophagy (an intracellular bulk degradation process for proteins and organelles) was significantly stimulated by myocardial I/R, but it was suppressed by BMPoC. Next, we examined how berbamine regulates autophagy and found that BMPoC inhibited the expression of beclin 1, a critical regulator for autophagosome initiation. Then, adenoviral overexpression and knockdown of beclin 1 in ventricles conformed its roles in the BMPoC-mediated cardioprotection. Further, Western blot analysis revealed that BMPoC-suppressed beclin 1 expression was mediated via the activation of PI3K/Akt signaling pathway. Our results suggest that BMPoC confers cardioprotection against I/R injury at least in part by the inhibition of beclin1-dependent autophagy through the activation of PI3K/Akt signaling pathway. These findings reveal new roles and mechanisms of berbamine in the cardioprotection against I/R injury.

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