Myocardial Hypertrophic Preconditioning Attenuates Cardiomyocyte Hypertrophy and Slows Progression to Heart Failure Through Upregulation of S100A8/A9

Xuan, Wei; Wu, Bing; Zhao, Jing; Zeng, Ziyue; Wang, Xuan; Cao, Shiping; Huang, Xiaobo; Asakura, Masanori; Xu, Dingli; Bin, Jianping; Kitakaze, Masafumi; Liao, Yulin

doi:10.1161/circulationaha.114.013789

Cited by 67 publications

(62 citation statements)

References 62 publications

(59 reference statements)

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“…At present, the methods of enhancing the anti‐OS ability of BMSCs mainly include the application of antioxidants or drugs, which mainly play a role through intervention of the signaling pathways of aging and apoptosis, but the effect is limited . Clinically, we often find that preconditioning has protective effects on organisms or body, such as myocardial ischemic preconditioning . That being so, whether OS preconditioning can also enhance anti‐OS ability of BMSCs, protect the survival of BMSCs under OS conditions?…”

Section: Introductionmentioning

confidence: 99%

New strategy of bone marrow mesenchymal stem cells against oxidative stress injury via Nrf2 pathway: oxidative stress preconditioning

Zhang

Peng

Zhang

et al. 2019

J of Cellular Biochemistry

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Clinically, bone marrow mesenchymal stem cells (BMSCs) have been used in treatment of many diseases, but the local oxidative stress (OS) of lesion severely limits the survival of BMSCs, which reduces the efficacy of BMSCs transplantation. Therefore, enhancing the anti-OS stress ability of BMSCs is a key breakthrough point. Preconditioning is a common protective mechanism for cells or body. Here, the aim of this study was to investigate the effects of OS preconditioning on the anti-OS ability of BMSCs and its mechanism.Fortunately, OS preconditioning can increase the expression of superoxide dismutase, catalase, NQO1, and heme oxygenase 1 through the nuclear factor erythroid 2-related factor 2 pathway, thereby decreased the intracellular reactive oxygen species (ROS) levels, relieved the damage of ROS to mitochondria, DNA and cell membrane, enhanced the anti-OS ability of BMSCs, and promoted the survival of BMSCs under OS.

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Section: Introductionmentioning

confidence: 99%

New strategy of bone marrow mesenchymal stem cells against oxidative stress injury via Nrf2 pathway: oxidative stress preconditioning

Zhang

Peng

Zhang

et al. 2019

J of Cellular Biochemistry

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“…The cellular hypertrophic response in cardiac myocytes appears to be an adaptational event and is well recognized to be responsible for several cardiovascular diseases such as heart failure and hypertrophic cardiomyopathy [25,26]. Ang II, one of the most common causes of myocardial hypertrophy, also plays a major role in the progression of myocardial hypertrophy to heart failure through signal transduction [1,27,28].…”

Section: Discussionmentioning

confidence: 99%

Transcriptional Effects of E3 Ligase Nrdp1 on Hypertrophy in Neonatal Rat Cardiomyocytes by Microarray and Integrated Gene Network Analysis

Zhang

Su²,

Zhang³

2016

Cardiology

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Objective: Neuregulin receptor degradation protein-1 (Nrdp1) is a novel E3 ubiquitin ligase, and we have previously shown that overexpression of Nrdp1 increased cardiomyocyte injury. However, the role of Nrdp1 in myocardial hypertrophy is unclear. In the present study, we clarified the molecular mechanisms of angiotensin II (Ang II)-induced cardiomyocyte hypertrophy regulated by Nrdp1 based on genome-wide transcriptional analysis. Methods: Neonatal rat cardiomyocytes were infected with adenoviruses containing green fluorescent protein (Ad-GFP) or wild-type Nrdp1 (Ad-Nrdp1), and then treated with Ang II for 36 h. Detection of differentially expressed genes was achieved with an Affymetrix Rat Gene 2.0 Array and Cluster and Java TreeView software. Results and Conclusion: Microarray data analysis demonstrated that Nrdp1 overexpression affected the expression of 12,140 mRNA genes in Ang II-induced cardiomyocyte hypertrophy, including the upregulation of 12,044 and the downregulation of 96. Gene ontology and globe signal transduction network analysis showed that Nrdp1 affected the expression of many genes related to stimulus response, the cell receptor pathway, and cell growth. Pathway network analysis identified myocardial metabolism, DNA replication, and the cell cycle as the most important pathways targeted by Nrdp1. lncRNA-mRNA coexpression network analysis showed that two core lncRNAs, NONRATT057160 and NONRATT054243, were involved in cardiomyotrophy regulated by Nrdp1 in cardiomyocytes. Taken together, these data provide compelling clues for further exploration of the function of Nrdp1 in heart disease.

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“…Suppression of the calcineurin/NFAT pathway by S100A8/A9 moderately causes the cardiac protection of hypertrophic preconditioning. 88 It has been reported that inhibition of nuclear factor (NF-kappa B) accenuates the cardio protective effect of ischemic preconditioning and reduces the infarct size during reperfusion. 89 Conversely, other have hypothesized that NF-kappa B have necessary and essential role in the development of compensatory and adaptive hypertrophy and its absence accelerates the remodeling process and functional development of heart failure.…”

Section: Impact Of Cardiac Hypertrophy On Ischemic Preconditioning Anmentioning

confidence: 99%

Abrogated cardio protective effect of ischemic preconditioning in hyperhomocysteinemia and hypertrophy

Qureshi

Goyal

2016

Journal of Indian College of Cardiology

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Myocardial Hypertrophic Preconditioning Attenuates Cardiomyocyte Hypertrophy and Slows Progression to Heart Failure Through Upregulation of S100A8/A9

Abstract: Supplemental Digital Content is available in the text.

Cited by 67 publications

References 62 publications

New strategy of bone marrow mesenchymal stem cells against oxidative stress injury via Nrf2 pathway: oxidative stress preconditioning

New strategy of bone marrow mesenchymal stem cells against oxidative stress injury via Nrf2 pathway: oxidative stress preconditioning

Transcriptional Effects of E3 Ligase Nrdp1 on Hypertrophy in Neonatal Rat Cardiomyocytes by Microarray and Integrated Gene Network Analysis

Abrogated cardio protective effect of ischemic preconditioning in hyperhomocysteinemia and hypertrophy

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