Microvascular function measurement in mice: From large to small

Matsunari, Ichiro

doi:10.1007/s12350-020-02097-1

Cited by 2 publications

(2 citation statements)

References 14 publications

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“…It is believed that the initial cause of coronary no-reflow injury is related to microvascular dysfunction [6]. The myocardial blood supply is composed of the subepicardial coronary artery and the capillaries that penetrate the myocardium [7], and microvessels form the main resistance to myocardial perfusion blood flow [8]. Further, coronary blood flow is inversely correlated with microvascular resistance.…”

Section: Introductionmentioning

confidence: 99%

Coronary Endothelium No‐Reflow Injury Is Associated with ROS‐Modified Mitochondrial Fission through the JNK‐Drp1 Signaling Pathway

Chen

Liu

Zhou

et al. 2021

Oxidative Medicine and Cellular Longevity

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Coronary artery no-reflow is a complex problem in the area of reperfusion therapy, and the molecular mechanisms underlying coronary artery no-reflow injury have not been fully elucidated. In the present study, we explored whether oxidative stress caused damage to coronary endothelial cells by inducing mitochondrial fission and activating the JNK pathway. The hypoxia/reoxygenation (H/R) model was induced in vitro to mimic coronary endothelial no-reflow injury, and mitochondrial fission, mitochondrial function, and endothelial cell viability were analyzed using western blotting, quantitative polymerase chain reaction (qPCR), enzyme-linked immunosorbent assay (ELISA), and immunofluorescence. Our data indicated that reactive oxygen species (ROS) were significantly induced upon H/R injury, and this was followed by decreased endothelial cell viability. Mitochondrial fission was induced and mitochondrial bioenergetics were impaired in cardiac endothelial cells after H/R injury. Neutralization of ROS reduced mitochondrial fission and protected mitochondrial function against H/R injury. Our results also demonstrated that ROS stimulated mitochondrial fission via JNK-mediated Drp1 phosphorylation. These findings indicate that the ROS-JNK-Drp1 signaling pathway may be one of the molecular mechanisms underlying endothelial cell damage during H/R injury. Novel treatments for coronary no-reflow injury may involve targeting mitochondrial fission and the JNK-Drp1 signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Coronary Endothelium No‐Reflow Injury Is Associated with ROS‐Modified Mitochondrial Fission through the JNK‐Drp1 Signaling Pathway

Chen

Liu

Zhou

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…The primary cause of coronary no‐reflow (NR) injury has been related to microvascular dysfunction (Zhou & Toan, 2020). The subepicardial coronary artery and the capillaries that enter the heart make up the coronary blood supply, and microvessels shape the essential barrier to myocardial perfusion blood float (Matsunari, 2020; Yue et al, 2010). Furthermore, microvascular resistance is inversely linked with coronary blood flow.…”

Section: Introductionmentioning

confidence: 99%

Shenlian extract decreases mitochondrial autophagy to regulate mitochondrial function in microvascular to alleviate coronary artery no‐reflow

Wang

et al. 2023

Phytotherapy Research

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Shenlian (SL) extract has been proven to be effective in the prevention and treatment of atherosclerosis and myocardial ischemia. However, the function and molecular mechanisms of SL on coronary artery no‐reflow have not been fully elucidated. This study was designed to investigate the contribution of SL extract in repressing excessive mitochondrial autophagy to protect the mitochondrial function and prevent coronary artery no‐reflow. The improvement of SL on coronary artery no‐reflow was observed in vivo experiments and the molecular mechanisms were further explored through vitro experiments. First, a coronary artery no‐reflow rat model was built by ligating the left anterior descending coronary artery for 2 hr of ischemia, followed by 24 hr of reperfusion. Thioflavin S (6%, 1 ml/kg) was injected into the inferior vena cava to mark the no‐reflow area. Transmission electron microscopy was performed to observe the cellular structure, mitochondrial structure, and mitochondrial autophagy of the endothelial cells. Immunofluorescence was used to observe the microvascular barrier function and microvascular inflammation. Cardiac microvascular endothelial cells (CMECs) were isolated from rats. The CMECs were deprived of oxygen–glucose deprivation (OGD) for 2 hr and reoxygenated for 4 hr to mimic the Myocardial ischemia‐reperfusion (MI/R) injury‐induced coronary artery no‐reflow in vitro. Mitochondrial membrane potential was assessed using JC‐1 dye. Intracellular adenosine triphosphate (ATP) levels were determined using an ATP assay kit. The cell total reactive oxygen species (ROS) levels and cell apoptosis rate were analyzed by flow cytometry. Colocalization of mitochondria and lysosomes indirectly indicated mitophagy. The representative ultrastructural morphologies of the autophagosomes and autolysosomes were also observed under transmission electron microscopy. The mitochondrial autophagy‐related proteins (LC3II/I, P62, PINK, and Parkin) were analyzed using Western blot analysis. In vivo, results showed that, compared with the model group, SL could reduce the no‐reflow area from 37.04 ± 9.67% to 18.31 ± 4.01% (1.08 g·kg−1 SL), 13.79 ± 4.77% (2.16 g·kg−1 SL), and 12.67 ± 2.47% (4.32 g·kg−1 SL). The extract also significantly increased the left ventricular ejection fraction (EF) and left ventricular fractional shortening (FS) (p < 0.05 or p < 0.01). The fluorescence intensities of VE‐cadherin, which is a junctional protein that preserves the microvascular barrier function, decreased to ~74.05% of the baseline levels in the no‐reflow rats and increased to 89.87%(1.08 g·kg−1SL), 82.23% (2.16 g·kg−1 SL), and 89.69% (4.32 g·kg−1 SL) of the baseline levels by SL treatment. SL administration repressed the neutrophil migration into the myocardium. The oxygen–glucose deprivation/reoxygenation (OGD/R) model was induced in vitro to mimic microvascular ischemia–reperfusion injury. The impaired mitochondrial function after OGD/R injury led to decreased ATP production, calcium overload, the excessive opening of the Mitochond...

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Microvascular function measurement in mice: From large to small

Cited by 2 publications

References 14 publications

Coronary Endothelium No‐Reflow Injury Is Associated with ROS‐Modified Mitochondrial Fission through the JNK‐Drp1 Signaling Pathway

Coronary Endothelium No‐Reflow Injury Is Associated with ROS‐Modified Mitochondrial Fission through the JNK‐Drp1 Signaling Pathway

Shenlian extract decreases mitochondrial autophagy to regulate mitochondrial function in microvascular to alleviate coronary artery no‐reflow

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