Poly (ADP-Ribose) Polymerase 1 Mediated Arginase II Activation Is Responsible for Oxidized LDL-Induced Endothelial Dysfunction

Wang, Qi; Zhao, Tong; Zhang, Wei; Yu, Wen-Bin; Liu, Bin; Wang, Zhao-Yang; Qiao, Wen; Lu, Qinghua; Wang, Aihua; Zhang, Mingxiang

doi:10.3389/fphar.2018.00882

Cited by 10 publications

(7 citation statements)

References 21 publications

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“…In mice, the overexpression of mitochondrial arginase II in endothelial cells reduces NO levels [ 112 ]. The loss of this equilibrium was also reported in the human endothelium with high levels of oxLDL, which cause an increase in arginase II activity [ 113 ].…”

Section: The Role Of Mitochondria In Atherosclerosismentioning

confidence: 69%

From Mitochondria to Atherosclerosis: The Inflammation Path

et al. 2021

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Inflammation is a key process in metazoan organisms due to its relevance for innate defense against infections and tissue damage. However, inflammation is also implicated in pathological processes such as atherosclerosis. Atherosclerosis is a chronic inflammatory disease of the arterial wall where unstable atherosclerotic plaque rupture causing platelet aggregation and thrombosis may compromise the arterial lumen, leading to acute or chronic ischemic syndromes. In this review, we will focus on the role of mitochondria in atherosclerosis while keeping inflammation as a link. Mitochondria are the main source of cellular energy. Under stress, mitochondria are also capable of controlling inflammation through the production of reactive oxygen species (ROS) and the release of mitochondrial components, such as mitochondrial DNA (mtDNA), into the cytoplasm or into the extracellular matrix, where they act as danger signals when recognized by innate immune receptors. Primary or secondary mitochondrial dysfunctions are associated with the initiation and progression of atherosclerosis by elevating the production of ROS, altering mitochondrial dynamics and energy supply, as well as promoting inflammation. Knowing and understanding the pathways behind mitochondrial-based inflammation in atheroma progression is essential to discovering alternative or complementary treatments.

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Section: The Role Of Mitochondria In Atherosclerosismentioning

confidence: 69%

From Mitochondria to Atherosclerosis: The Inflammation Path

et al. 2021

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“…VECs maintain intravascular homeostasis mainly by regulating vascular relaxation, leukocyte adhesion, platelet activation, and smooth muscle cell proliferation and migration (37,38). The first pathophysiological change is endothelial dysfunction in the early stage of AS, which characterized by the decrease of NO synthesis and secretion (39).…”

Section: Discussionmentioning

confidence: 99%

LncRNA FENDRR Inhibits ox-LDL Induced Mitochondrial Energy Metabolism Disorder in Aortic Endothelial Cells via miR-18a-5p/PGC-1α Signaling Pathway

Wang

Yang

et al. 2021

Front. Endocrinol.

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Atherosclerosis (AS) is the main cause of morbidity and mortality in the world. Mitochondrial dysfunction is closely related to AS. At present, several signaling pathways related to mitochondrial dysfunction have been found, one of which is around PGC-1α. PGC-1α is a transcription activator, which is related to mitochondrial biogenesis and antioxidant defense. In this study, we explored the effect of miR-18a-5p/PGC-1α signaling pathway on mitochondrial energy metabolism in HAECs with ox-LDL treatment. The results showed that the mitochondrial energy metabolism disorder in HAECs treated by ox-LDL was related to the downregulation of LncRNA FENDRR and PGC-1α. FENDRR could reverse ox-LDL induced mitochondrial energy metabolism disorder and upregulate the PGC-1α expression. FENDRR could be used as ceRNA to inhibit the miR-18a-5p expression and reduce the negative regulation of miR-18a-5p on PGC-1α. Downregulation of miR-18a-5p expression or upregulation of PGC-1α in ox-LDL treated HAECs could reverse mitochondrial energy metabolism disorder. In conclusion, these findings suggested that FENDRR/miR-18a-5p/PGC-1α signaling pathway regulated mitochondrial energy metabolism in HAECs; ox-LDL downregulated the expression of PGC-1α and cause mitochondrial energy metabolism disorder by inhibiting this signal pathway.

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“…Zhang et al found that ox-LDL can induce coronary EC damage that is independent of caspase but dependent on the nuclear translocation of AIF (113). Wang et al found that PARP1 was a key factor in the upregulation of arginase II (Arg II) induced by ox-LDL (114). Arg II results in reduced NO synthesis by competing with eNOS for the same substrate, l-arginine (115)(116)(117).…”

Section: Ros Trigger Parthanatos In Ecsmentioning

confidence: 99%

“…Arg II results in reduced NO synthesis by competing with eNOS for the same substrate, l-arginine (115)(116)(117). PARP1 deficiency results in suppressed Arg II expression, enhanced eNOS expression, and improved NO production and endothelial function (114). Choi et al found that enhanced PARP-1 activity is closely related to coronary artery endothelial dysfunction in mice with type 2 diabetes.…”

Section: Ros Trigger Parthanatos In Ecsmentioning

confidence: 99%

ROS-triggered endothelial cell death mechanisms: Focus on pyroptosis, parthanatos, and ferroptosis

Zheng

Liu²,

Piao³

et al. 2022

Front. Immunol.

123

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The endothelium is a single layer of epithelium covering the surface of the vascular system, and it represents a physical barrier between the blood and vessel wall that plays an important role in maintaining intravascular homeostasis. However, endothelial dysfunction or endothelial cell death can cause vascular barrier disruption, vasoconstriction and diastolic dysfunction, vascular smooth muscle cell proliferation and migration, inflammatory responses, and thrombosis, which are closely associated with the progression of several diseases, such as atherosclerosis, hypertension, coronary atherosclerotic heart disease, ischemic stroke, acute lung injury, acute kidney injury, diabetic retinopathy, and Alzheimer’s disease. Oxidative stress caused by the overproduction of reactive oxygen species (ROS) is an important mechanism underlying endothelial cell death. Growing evidence suggests that ROS can trigger endothelial cell death in various ways, including pyroptosis, parthanatos, and ferroptosis. Therefore, this review will systematically illustrate the source of ROS in endothelial cells (ECs); reveal the molecular mechanism by which ROS trigger pyroptosis, parthanatos, and ferroptosis in ECs; and provide new ideas for the research and treatment of endothelial dysfunction-related diseases.

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Poly (ADP-Ribose) Polymerase 1 Mediated Arginase II Activation Is Responsible for Oxidized LDL-Induced Endothelial Dysfunction

Cited by 10 publications

References 21 publications

From Mitochondria to Atherosclerosis: The Inflammation Path

From Mitochondria to Atherosclerosis: The Inflammation Path

LncRNA FENDRR Inhibits ox-LDL Induced Mitochondrial Energy Metabolism Disorder in Aortic Endothelial Cells via miR-18a-5p/PGC-1α Signaling Pathway

ROS-triggered endothelial cell death mechanisms: Focus on pyroptosis, parthanatos, and ferroptosis

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