Ischemia and reperfusion related myocardial inflammation: A network of cells and mediators targeting the cardiomyocyte

Rohrbach, Susanne; Troidl, Christian; Hamm, Christian W.; Schulz, Rainer

doi:10.1002/iub.1352

Cited by 30 publications

(18 citation statements)

References 144 publications

(160 reference statements)

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“…Monocyte/macrophage infiltration after myocardial infarction has been confirmed, suggesting that inhibition of excessive inflammation could limit IS and strengthen heart function [29]. Studies have confirmed that PD has anti-inflammatory effects via inhibiting expression of interleukin-17 [30] and various cell adhesion molecules [31].…”

Section: Discussionmentioning

confidence: 95%

Polydatin post-treatment alleviates myocardial ischaemia/reperfusion injury by promoting autophagic flux

et al. 2016

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Polydatin (PD), a resveratrol (RES) glycoside, has a stronger antioxidative effect than RES. It is known that RES is an autophagic enhancer and exerts a cardioprotective effect against ischaemia/reperfusion (I/R) injury. However, the effect of PD post-treatment on myocardial I/R injury remains unclear. In the present study, we investigated the influences of PD post-treatment on myocardial I/R injury and autophagy. C57BL/6 mice underwent left coronary artery (LCA) occlusion and cultured neonatal rat cardiomyocytes (NRCs) subjected to hypoxia were treated with vehicle or PD during reperfusion or re-oxygenation. We noted that PD enhanced autophagy and decreased apoptosis during I/R or hypoxia/reoxygenation (H/R), and this effect was antagonized by co-treatment with adenovirus carrying short hairpin RNA for Beclin 1 and 3-methyladenine (3-MA), an autophagic inhibitor. Compared with vehicle-treated mice, PD-treated mice had a significantly smaller myocardial infarct size (IS) and a higher left ventricular fractional shortening (LVFS) and ejection fraction (EF), whereas these effects were partly reversed by 3-MA. Furthermore, in the PD-treated NRCs, tandem fluorescent mRFP-GFP-LC3 assay showed abundant clearance of autophagosomes with an enhanced autophagic flux, and co-treatment with Bafilomycin A1 (Baf), a lysosomal inhibitor, indicated that PD promoted the degradation of autolysosome. In addition, PD post-treatment reduced mitochondrial membrane potential and cellular reactive oxygen species (ROS) production in NRCs, and these effects were partially blocked by Baf. These findings indicate that PD post-treatment limits myocardial I/R injury by promoting autophagic flux to clear damaged mitochondria to reduce ROS and cell death.

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Section: Discussionmentioning

confidence: 95%

Polydatin post-treatment alleviates myocardial ischaemia/reperfusion injury by promoting autophagic flux

et al. 2016

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“…Myocardial ischemia/reperfusion‐related heart diseases are major causes of heart failure, and exploring the novel molecules to reduce MIRI has been a topic of intense investigation . There is growing evidence that CMECs play a critical role in myocardial I/R progression . Thus, it is crucial to investigate the protection of CMECs against H/R to reduce MIRI.…”

Section: Discussionmentioning

confidence: 99%

“…20 There is growing evidence that CMECs play a critical role in myocardial I/R progression. 21,22 Thus, it is crucial to investigate the protection of CMECs against H/R to reduce MIRI. Recent studies indicated that Tβ4 could improve cardiac function after myocardial ischemic injury.…”

Section: Cmecs Injury Through the Mir-200a-nrf2 Pathwaymentioning

confidence: 99%

miR‐200a mediates protection of thymosin β‐4 in cardiac microvascular endothelial cells as a novel mechanism under hypoxia‐reoxygenation injury

Zhu

Liu

et al. 2019

J of Cellular Biochemistry

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Thymosin β‐4 (Tβ4) is a ubiquitous protein, which has been suggested to regulate multiple cell signal pathways and a variety of cellular functions. However, the role Tβ4 plays in the cardiac microvascular endothelial cells (CMECs) under myocardial ischemia/reperfusion injury is currently unknown. Here we investigated the effects of Tβ4 on hypoxia/reoxygenation (H/R) induced CMECs injury and its potential molecular mechanism. Cultured CMECs were positively identified by flow cytometry using antibody against CD31 and VWF/Factor VIII, which are constitutively expressed on the surface of CMECs. Then the reduced level of Tβ4 was detected in H/R‐CMECs by a real‐time quantitative polymerase chain reaction. To determine the effects of Tβ4 on H/R‐CMECs, we transfected the overexpression or silence vector of Tβ4 into CMECs under H/R condition. Our results indicated that H/R treatment could reduce proliferation, increased apoptosis, adhesion, and reactive oxygen species (ROS) production in CMECs, which were attenuated by Tβ4 overexpression or aggravated by Tβ4 silencing, implying Tβ4 is able to promote CMECs against H/R‐induced cell injury. Furthermore, the microRNA‐200a (miR‐200a) level was also increased by Tβ4 in H/R‐CMECs or reduced by Tβ4 small interfering RNA. To investigated the mechanism of protective effects of Tβ4 on CMECs injury, the miR‐200a inhibitor was transfected into H/R‐CMECs. The results indicated that inhibition of miR‐200a inversed the protection of Tβ4 on H/R‐CMECs, specifically including cell proliferation, cell adhesion, cell apoptosis, and ROS production, as well as nuclear factor erythroid 2‐related factor 2 (Nrf2) nuclear translocation. In conclusion, our results determined that Tβ4 attenuated H/R‐induced CMECs injury by miR‐200a‐Nrf2 signaling.

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“…A growing body of evidence shows that CMECs play a unique and critical role in myocardial I/R progression (Anversa et al, 1980; Brutsaert, 2003; Rohrbach et al, 2015). It is crucial to maintain its integrity and function of the microvascular endothelium in order to reduce myocardial I/R injury.…”

Section: Discussionmentioning

confidence: 99%

N-n-butyl Haloperidol Iodide Protects against Hypoxia/Reoxygenation Injury in Cardiac Microvascular Endothelial Cells by Regulating the ROS/MAPK/Egr-1 Pathway

Zhang

Zhong

et al. 2017

Front. Pharmacol.

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Endothelium dysfunction induced by reactive oxygen species (ROS) is an important initial event at the onset of myocardial ischemia/reperfusion in which the Egr-1 transcription factor often serves as a master switch for various damage pathways following reperfusion injury. We hypothesized that an intracellular ROS/MAPK/Egr-1 signaling pathway is activated in cardiac microvascular endothelial cells (CMECs) following hypoxia/reoxygenation (H/R). ROS generation, by either H/R or the ROS donor xanthine oxidase-hypoxanthine (XO/HX) activated all three MAPKs (ERK1/2, JNK, p38), and induced Egr-1 expression and Egr-1 DNA-binding activity in CMECs, whereas ROS scavengers (EDA and NAC) had the opposite effect following H/R. Inhibitors of all three MAPKs individually inhibited induction of Egr-1 expression by H/R in CMECs. Moreover, N-n-butyl haloperidol (F2), previously shown to protect cardiomyocytes subjected to I/R, dose-dependently downregulated H/R-induced ROS generation, MAPK activation, and Egr-1 expression and activity in CMECs, whereas XO/HX and MAPK activators (EGF, anisomycin) antagonized the effects of F2. Inhibition of the ROS/MAPK/Egr-1 signaling pathway, by either F2, NAC, or inhibition of MAPK, increased CMEC viability and the GSH/GSSG ratio, and decreased Egr-1 nuclear translocation. These results show that the ROS/MAPK/Egr-1 signaling pathway mediates H/R injury in CMECs, and F2 blocks this pathway to protect against H/R injury and further alleviate myocardial I/R injury.

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Ischemia and reperfusion related myocardial inflammation: A network of cells and mediators targeting the cardiomyocyte

Cited by 30 publications

References 144 publications

Polydatin post-treatment alleviates myocardial ischaemia/reperfusion injury by promoting autophagic flux

Polydatin post-treatment alleviates myocardial ischaemia/reperfusion injury by promoting autophagic flux

miR‐200a mediates protection of thymosin β‐4 in cardiac microvascular endothelial cells as a novel mechanism under hypoxia‐reoxygenation injury

N-n-butyl Haloperidol Iodide Protects against Hypoxia/Reoxygenation Injury in Cardiac Microvascular Endothelial Cells by Regulating the ROS/MAPK/Egr-1 Pathway

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