Synergistic effect of atorvastatin and cyanidin-3-glucoside against angiotensin II-mediated vascular smooth muscle cell proliferation and migration through MAPK and PI3K/Akt pathways

Pantan, Rungusa; Tocharus, Jiraporn; Phatsara, Manussabhorn; Suksamrarn, Apichart; Tocharus, Chainarong

doi:10.1007/s12272-016-0836-3

Cited by 4 publications

(6 citation statements)

References 40 publications

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“…Here, we used a model of HA-VSMC senescence induced by Ang II and verified that senescent HA-VSMCs enhanced migration and invasion, which was in agreement with previous reports regarding increasing migratory and invasive capacities in senescent rat VSMCs (24,37). Furthermore, it has been shown that Ang II can stimulate VSMC migration and invasion measured by a wound healing approach and Boyden chamber assay (20,21).…”

Section: Discussionsupporting

confidence: 90%

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Serum containing Buyang Huanwu decoction prevents age-associated migration and invasion of human vascular smooth muscle cells by up regulating SIRT1 expression

Zhang

Wei

Ruan

et al. 2018

BST

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Section: Discussionsupporting

confidence: 90%

“…Ang II is a major inductor of VSMCs senescence, and has been shown to potently simulate VSMCs migration and invasion (17)(18)(19)(20)(21). In addition, inhibition of Ang II pathways has been shown to substantially reduce ageassociated arterial remodeling (3,4).…”

Section: Introductionmentioning

confidence: 99%

Serum containing Buyang Huanwu decoction prevents age-associated migration and invasion of human vascular smooth muscle cells by up regulating SIRT1 expression

Zhang

Wei

Ruan

et al. 2018

BST

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“…Accumulated evidence shows PI3K phosphorylates Akt at Ser473 causing the kinase to be activated, and to mediate downstream signaling processes associated with cell growth and migration 44, 55–58 , but has also been implicated in endothelium-dependent relaxation 41, 42 . More pertinently, eNOS has been found to be activated via the PI3K/Akt pathway by natural compounds like epigallocatechin-3-gallate 59 .…”

Section: Discussionmentioning

confidence: 99%

Salvia fruticosa Induces Vasorelaxation In Rat Isolated Thoracic Aorta: Role of the PI3K/Akt/eNOS/NO/cGMP Signaling Pathway

Anwar

Samaha

Ballan

et al. 2017

Sci Rep

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Salvia fruticosa (SF) Mill. is traditionally used for its antihypertensive actions. However, little is known about its pharmacologic and molecular mechanisms of action. Here we determined the effects of an ethanolic extract of SF leaves on rings of isolated thoracic aorta from Sprague-Dawley rats. Our results show that SF extract increased nitric oxide production and relaxed endothelium-intact rings in a dose-dependent (0.3 µg/ml–1 mg/ml) manner, and the maximum arterial relaxation (Rmax) was significantly reduced with endothelium denudation. Pretreatment of endothelium-intact rings with L-NAME (a non-selective inhibitor of nitric oxide synthase, 100 µM), or ODQ (an inhibitor of soluble guanylyl cyclase, 10 µM) significantly diminished SF-mediated vasorelaxation. Furthermore, SF induced Akt phosphorylation as well as increased cGMP levels in rings treated with increasing doses of SF. Prior exposure to PI3K inhibitors, wortmannin (0.1 µM) or LY294002 (10 µM), decreased cGMP accumulation and attenuated the SF-induced vasorelaxation by approximately 50% (Rmax). SF-evoked relaxation was not affected by indomethacin, verapamil, glibenclamide, tetraethylammonium, pyrilamine or atropine. Taken together, our results indicate that SF induces endothelium-dependent vasorelaxation through the PI3K/Akt/eNOS/NO/sGC/cGMP signaling pathway. Our data illustrate the health-orientated benefits of consuming SF which may act as an antihypertensive agent to reduce the burden of cardiovascular complications.

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“…The synergistic effects of atorvastatin and cyanidin-3-glucoside improves HASMC proliferation and migration by enhancing cell cycle arrest through the AT 1R-mediated MAPK and PI3K/Akt pathways ( Pantan et al, 2016 ). FOXO3a phosphorylation plays an important role in mediating MMP-2 activation and VSMC migration.…”

Section: Pi3k-targeted Therapy In Atherosclerosismentioning

confidence: 99%

Role of PI3K in the Progression and Regression of Atherosclerosis

et al. 2021

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Phosphatidylinositol 3 kinase (PI3K) is a key molecule in the initiation of signal transduction pathways after the binding of extracellular signals to cell surface receptors. An intracellular kinase, PI3K activates multiple intracellular signaling pathways that affect cell growth, proliferation, migration, secretion, differentiation, transcription and translation. Dysregulation of PI3K activity, and as aberrant PI3K signaling, lead to a broad range of human diseases, such as cancer, immune disorders, diabetes, and cardiovascular diseases. A growing number of studies have shown that PI3K and its signaling pathways play key roles in the pathophysiological process of atherosclerosis. Furthermore, drugs targeting PI3K and its related signaling pathways are promising treatments for atherosclerosis. Therefore, we have reviewed how PI3K, an important regulatory factor, mediates the development of atherosclerosis and how targeting PI3K can be used to prevent and treat atherosclerosis.

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Synergistic effect of atorvastatin and cyanidin-3-glucoside against angiotensin II-mediated vascular smooth muscle cell proliferation and migration through MAPK and PI3K/Akt pathways

Cited by 4 publications

References 40 publications

Serum containing Buyang Huanwu decoction prevents age-associated migration and invasion of human vascular smooth muscle cells by up regulating SIRT1 expression

Serum containing Buyang Huanwu decoction prevents age-associated migration and invasion of human vascular smooth muscle cells by up regulating SIRT1 expression

Salvia fruticosa Induces Vasorelaxation In Rat Isolated Thoracic Aorta: Role of the PI3K/Akt/eNOS/NO/cGMP Signaling Pathway

Role of PI3K in the Progression and Regression of Atherosclerosis

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