Nucleolin mediated pro‐angiogenic role of Hydroxysafflor Yellow A in ischaemic cardiac dysfunction: Post‐transcriptional regulation of <scp>VEGF</scp>‐A and <scp>MMP</scp>‐9

Zou, Jian; Wang, Nian; Liu, Manting; Bai, Yongping; Wang, Hao; Liu, Ke; Zhang, Huali; Xiao, Xianzhong; Wang, Kangkai

doi:10.1111/jcmm.13552

Cited by 45 publications

(39 citation statements)

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“…Therefore, the changes of VEGF-A content, angiogenesis, ER stress, and autophagy in the endothelial cells of ischemic myocardium in the AMI mice were first determined, and then in vitro studies were performed to analyze the role of ER stress and autophagy in VEGF-Ainduced angiogenesis and the potential mechanisms. A mouse model of AMI was established by occlusion of the left anterior descending coronary artery according to the procedure we previously reported (Zou et al, 2018).…”

mentioning

confidence: 99%

VEGF‐A promotes angiogenesis after acute myocardial infarction through increasing ROS production and enhancing ER stress‐mediated autophagy

Zou

Qin

et al. 2019

Journal Cellular Physiology

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142

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Proangiogenesis is generally regarded as an effective approach for treating ischemic heart disease. Vascular endothelial growth factor (VEGF)‐A is a strong and essential proangiogenic factor. Reactive oxygen species (ROS), endoplasmic reticulum (ER) stress, and autophagy are implicated in the process of angiogenesis. This study is designed to clarify the regulatory mechanisms underlying VEGF‐A, ROS, ER stress, autophagy, and angiogenesis in acute myocardial infarction (AMI). A mouse model of AMI was successfully established by occluding the left anterior descending coronary artery. Compared with the sham‐operated mice, the microvessel density, VEGF‐A content, ROS production, expression of vascular endothelial cadherin, positive expression of 78 kDa glucose‐regulated protein/binding immunoglobulin protein (GRP78/Bip), and LC3 puncta in CD31‐positive endothelial cells of the ischemic myocardium were overtly elevated. Moreover, VEGF‐A exposure predominantly increased the expression of beclin‐1, autophagy‐related gene (ATG) 4, ATG5, inositol‐requiring enzyme‐1 (IRE‐1), GRP78/Bip, and LC3‐II/LC3‐I as well as ROS production in the human umbilical vein endothelial cells (HUVECs) in a dose and time‐dependent manner. Both beclin‐1 small interfering RNA and 3‐methyladenine treatment predominantly mitigated VEGF‐A‐induced tube formation and migration of HUVECs, but they failed to elicit any notable effect on VEGF‐A‐increased expression of GRP78/Bip. Tauroursodeoxycholic acid not only obviously abolished VEGF‐A‐induced increase of IRE‐1, GRP78/Bip, beclin‐1 expression, and LC3‐II/LC3‐I, but also negated VEGF‐A‐induced tube formation and migration of HUVECs. Furthermore, N‐acetyl‐ l‐cysteine markedly abrogated VEGF‐A‐increased ROS production, IRE‐1, GRP78/Bip, beclin‐1 expression, and LC3‐II/LC3‐I in the HUVECs. Taken together, our data demonstrated that increased spontaneous production of VEGF‐A may induce angiogenesis after AMI through initiating ROS–ER stress‐autophagy axis in the vascular endothelial cells.

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mentioning

confidence: 99%

VEGF‐A promotes angiogenesis after acute myocardial infarction through increasing ROS production and enhancing ER stress‐mediated autophagy

Zou

Qin

et al. 2019

Journal Cellular Physiology

Self Cite

142

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“…It was confirmed that SYA could protect neonatal rat cardiomyocytes against anoxia/reoxygenation injury in vitro [34]. There have been a large number of studies showing the protective effects of HSYA on the cardiovascular system [35][36][37], nervous system [38,39], liver [40,41], lung [42,43], and others. It was also found to inhibit certain tumors [44,45] and has a certain impact on metabolism [46].…”

Section: Discussionmentioning

confidence: 86%

Three Ingredients of Safflower Alleviate Acute Lung Injury and Inhibit NET Release Induced by Lipopolysaccharide

Wang

Guo

Wen

et al. 2020

Mediators of Inflammation

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Xuebijing injection is a Chinese herb compound to treat sepsis in China, but it contains many different kinds of components, and each component may have different effects in treating sepsis. The present study was performed to investigate the effect of three ingredients of Xuebijing, safflor yellow A (SYA), hydroxysafflor yellow A (HSYA), and anhydrosafflor yellow B (AHSYB), in lipopolysaccharide- (LPS-) induced acute lung injury (ALI). LPS (10 mg/kg) was injected intratracheally to induce acute lung injury in mice, which were then treated with SYA, HSYA, and AHSYB. The blood, bronchoalveolar lavage fluid (BALF), and lung tissues were collected to detect degree of lung injury, level of inflammation, and neutrophil extracellular traps (NETs). In vitro experiments were performed using HL-60 cells stimulated with phorbol myristate acetate (PMA). Lung injury induced by LPS was alleviated by SYA, HSYA, and AHSYB as demonstrated by the histopathologic test. The three components inhibit LPS-induced elevation of the levels of inflammatory factors and wet-to-dry weight ratio as well as the amount of protein and cells in the BALF. They also induced a remarkably less overlay of myeloperoxidase (MPO) and histone in the immunofluorescence assay and reduced level of MPO-DNA complex in plasma. The in vitro assay showed a similar trend that the three components inhibited PMA-induced NET release in neutrophil-like HL-60 cells. Western blot demonstrated that phosphorylation of c-rapidly accelerated fibrosarcoma (c-Raf), mitogen-activated protein kinase ERK kinase (MEK), and extracellular signal-regulated kinase (ERK) in the lungs of LPS-challenged mice, and PMA-treated HL-60 cells were all significantly reduced by SYA, HSYA, and AHSYB. Therefore, our data demonstrated that three components of XBJ, including SYA, HSYA, and AHSYB, showed a protective effect against LPS-induced lung injury and NET release.

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“…Meanwhile, cells with high glucose showed no signi cant changes compared to control group, illustrating the non-cytotoxic effect of 30 mM glucose concentration. The initial process of angiogenesis is the organization of individual endothelial cells into a 3-dimensional tube-like structure [51]. RAECs were seeded on the basement membrane matrix.…”

Section: L-arginine and Vitamin C Enhanced Angiogenesis In Raecsmentioning

confidence: 99%

Improvement of cardiac dysfunction by L-arginine combined with vitamin C through restoring angiogenesis associated with NADPH/NOS/NO signal pathway in diabetic rats

Cai

et al. 2020

Preprint

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Background In diabetic patients, the occurrence of ischemic events such as myocardial infarction is significantly higher than that of normal patients. L-arginine and vitamin C are commonly used adjuvant drugs in clinical practice. But whether L-arginine and vitamin C can be used together, the role of promoting angiogenesis to improve vascular dysfunction and its mechanism of action are not clear. To this end, we investigated whether L-arginine in combination with vitamin C promotes revascularization after myocardial infarction in patients with type 2 diabetes by inhibiting angiogenesis disorders associated with NADPH oxidase. Methods Experimental myocardial infarction (MI) was induced by left anterior descending coronary artery ligation in diabetic Sprague-Dawley rats and non-diabetic controls. Cardiac function was studied by echocardiography and LDH activity. Western blotting was used to study VEGF, Nox4, Nox1, Nox2, eNOS and phospho-eNOS (Ser1177), CAT-1. Angiogenesis, cell proliferation and migration were detected by micro-vessel density assay, cell viability assay, scratch wound-healing assay and tube formation assay. Results First, we cultured rat aortic endothelial cells in a high glucose environment for 48 hours, then treated L-arginine and vitamin C alone or together. It was shown that high glucose significantly damaged cell proliferation, migration and tube formation, which was normalized by L-arginine with vitamin C combined application. Furthermore, we found that co-treatment of L-arginine and vitamin C activated NOS/NO signaling pathway via inhibited NADPH oxidase activity, which regulated angiogenesis in RAECs. In vivo, L-arginine and vitamin C co-intervention improved cardiac function by implementing echocardiographic examination and LDH activity. This therapy also relieved the vasodilatory response to acetylcholine and restored the expressions of p-eNOS and VEGF, together with reducing Nox2 and iNOS production in the ischemic myocardium of high-fat diet (HFD)-fed rats following streptozocin (STZ) injection. Conclusion Overall, for the first time, this study reveals that the combination of L-arginine and vitamin C restores the blood supply to myocardial infarction in rats with type 2 diabetes by promoting angiogenesis, which was attributed to activating NOS/NO signaling pathway via blocking NADPH-dependent O2− generation.

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Nucleolin mediated pro‐angiogenic role of Hydroxysafflor Yellow A in ischaemic cardiac dysfunction: Post‐transcriptional regulation of VEGF‐A and MMP‐9

Cited by 45 publications

References 44 publications

VEGF‐A promotes angiogenesis after acute myocardial infarction through increasing ROS production and enhancing ER stress‐mediated autophagy

VEGF‐A promotes angiogenesis after acute myocardial infarction through increasing ROS production and enhancing ER stress‐mediated autophagy

Three Ingredients of Safflower Alleviate Acute Lung Injury and Inhibit NET Release Induced by Lipopolysaccharide

Improvement of cardiac dysfunction by L-arginine combined with vitamin C through restoring angiogenesis associated with NADPH/NOS/NO signal pathway in diabetic rats

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