Macrophage-mediated regulation of catecholamines in sympathetic neural remodeling after myocardial infarction

Lyu, Jingjing; Wang, Man; Kang, Xinjiang; Xu, Hua‐Dong; Cao, Zhongming; Yu, Tao; Huang, Keli; Wu, Jin; Wei, Xin; Qian, Lei

doi:10.1007/s00395-020-0813-3

Cited by 29 publications

(20 citation statements)

References 56 publications

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“…To better simulate acute myocardial infarction, we set the infarct time between 1 and 7 days. 15 The expectation was that we would identify new targets for the treatment of acute myocardial infarction or that we would identify pathways to advance relevant research.…”

Section: Discussionmentioning

confidence: 99%

<p>Screening and Identification of Potential Hub Genes in Myocardial Infarction Through Bioinformatics Analysis</p>

Xue

Qian

et al. 2020

CIA

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Background: Myocardial infarction (MI) is a common cause of death worldwide. It is characterized by coronary artery occlusion that causes ischemia and hypoxia of myocardial cells, leading to irreversible myocardial damage. Materials and Methods: To explore potential targets for treatment of MI, we reorganized and analyzed two microarray datasets (GSE4648 and GSE775). The GEO2R tool was used to screen for differentially expressed genes (DEGs) between infarcted and normal myocardium. We used the Database for Annotation, Visualization and Integrated Discovery (DAVID) to perform Gene Ontology functional annotation analysis (GO analysis) and the Kyoto Encyclopedia of Genes and Genomes for pathway enrichment analysis (KEGG analysis). We examined protein-protein interactions to characterize the relationship between differentially expressed genes, and we screened potential hub genes according to the degree of connection. PCR and Western blotting were used to identify the core genes. Results: At different times of infarction, a total of 35 genes showed upregulation at all times; however, none of the genes showed downregulation at all 3 times. Similarly, 10 hub genes with high degrees of connectivity were identified. In vivo and in vitro experiments suggested that expression levels of MMP-9 increased at various times after myocardial infarction and that expression increased in a variety of cells simultaneously. Conclusion: Expression levels of MMP-9 increase throughout the course of acute myocardial infarction, and this expression has both positive and negative sides. Further studies are needed to explore the role of MMP-9 in MI treatment. The potential values of Il6,

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Section: Discussionmentioning

confidence: 99%

<p>Screening and Identification of Potential Hub Genes in Myocardial Infarction Through Bioinformatics Analysis</p>

Xue

Qian

et al. 2020

CIA

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“…15596026). RNA was quantified, and quality was determined by using BioDrop (Biochrom, UK) [ 39 , 40 ]. Total RNA (1 μ g) was reverse transcribed and real-time PCR analysis using Fast SYBRTM Green Master Mix (Applied Biosystems, Cat No.…”

Section: Methodsmentioning

confidence: 99%

[Retracted] Melatonin Attenuates Cardiac Ischemia‐Reperfusion Injury through Modulation of IP3R‐Mediated Mitochondria‐ER Contact

Liu

Wang

et al. 2021

Oxidative Medicine and Cellular Longevity

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Although the interplay between mitochondria and ER has been identified as a crucial regulator of cellular homeostasis, the pathogenic impact of alterations in mitochondria-ER contact sites (MERCS) during myocardial postischemic reperfusion (I/R) injury remains incompletely understood. Therefore, in our study, we explored the beneficial role played by melatonin in protecting cardiomyocytes against reperfusion injury via stabilizing mitochondria-ER interaction. In vitro exposure of H9C2 rat cardiomyocytes to hypoxia/reoxygenation (H/R) augmented mitochondrial ROS synthesis, suppressed both mitochondrial potential and ATP generation, and increased the mitochondrial permeability transition pore (mPTP) opening rate. Furthermore, H/R exposure upregulated the protein content of CHOP and caspase-12, two markers of ER stress, and enhanced the transcription of main MERCS tethering proteins, namely, Fis1, BAP31, Mfn2, and IP3R. Interestingly, all the above changes could be attenuated or reversed by melatonin treatment. Suggesting that melatonin-induced cardioprotection works through normalization of mitochondria-ER interaction, overexpression of IP3R abolished the protective actions offered by melatonin on mitochondria-ER fitness. These results expand our knowledge on the cardioprotective actions of melatonin during myocardial postischemic reperfusion damage and suggest that novel, more effective treatments for acute myocardial reperfusion injury might be achieved through modulation of mitochondria-ER interaction in cardiac cells.

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“…Cells (1 × 10 5 cells) were plated in a 24-well plate and transfected with siRNA. Fortyeight hours after transfection, FACS (BD FACSAria TM II, BD) was performed to isolate GFP-positive cells [39]. Following isolation, cells were plated in a 96-well plate by limiting dilution for a single-cell cloning.…”

Section: Generation Of Yap Knockout Cell Line Sirna Againstmentioning

confidence: 99%

Yap-Hippo Signaling Activates Mitochondrial Protection and Sustains Breast Cancer Viability under Hypoxic Stress

Chen

Zhang

Guo

et al. 2021

Journal of Oncology

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Yes-associated protein (Yap) is a transcriptional regulator that upregulates oncogenes and downregulates tumor repressor genes. In this study, we analyzed protein expression, RNA transcription, and signaling pathways to determine the function and mechanism of Yap in breast cancer survival during hypoxic stress. Yap transcription was drastically upregulated by hypoxia in a time-dependent manner. siRNA-mediated Yap knockdown attenuated breast cancer viability and impaired cell proliferation under hypoxic conditions. Yap knockdown induced mitochondrial stress, including mitochondrial membrane potential reduction, mitochondrial oxidative stress, and ATP exhaustion after exposure to hypoxia. It also repressed mitochondrial protective systems, including mitophagy and mitochondrial fusion upon exposure to hypoxia. Finally, our data showed that Yap knockdown suppresses MCF-7 cell migration by inhibiting F-actin transcription and promoting lamellipodium degradation under hypoxic stress. Taken together, Yap maintenance of mitochondrial function and activation of F-actin/lamellipodium signaling is required for breast cancer survival, migration, and proliferation under hypoxic stress.

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Macrophage-mediated regulation of catecholamines in sympathetic neural remodeling after myocardial infarction

Cited by 29 publications

References 56 publications

<p>Screening and Identification of Potential Hub Genes in Myocardial Infarction Through Bioinformatics Analysis</p>

<p>Screening and Identification of Potential Hub Genes in Myocardial Infarction Through Bioinformatics Analysis</p>

[Retracted] Melatonin Attenuates Cardiac Ischemia‐Reperfusion Injury through Modulation of IP3R‐Mediated Mitochondria‐ER Contact

Yap-Hippo Signaling Activates Mitochondrial Protection and Sustains Breast Cancer Viability under Hypoxic Stress

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