Tropoelastin Enhances Nitric Oxide Production by Endothelial Cells

Hiob, Matti A.; Trane, Andy; Wise, Steven G.; Bernatchez, Pascal; Weiss, Anthony S.

doi:10.2217/nnm-2016-0052

Cited by 10 publications

(10 citation statements)

References 34 publications

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“…Robinet et al [ 5 ] stated that κ-elastin and the VGVAPG peptide increased NO production in rat cardiomyocytes (RCs) and human coronary artery endothelial cells (HCAECs) [ 5 ]. Similarly, VGVAPG and tropoelastin also increased NO production in HMEC and bovine aortic endothelial cells (BAECs), respectively [ 31 , 41 ]. However, in the brain in the early stages of haemorrhage and ischaemic stroke, a global decrease in the NO level occurs and corresponds to an increase in P-selectin levels, which promotes platelet aggregation and fibrin deposition and leads to microthrombosis formation [ 42 ].…”

Section: Discussionmentioning

confidence: 99%

The VGVAPG Peptide Regulates the Production of Nitric Oxide Synthases and Reactive Oxygen Species in Mouse Astrocyte Cells In Vitro

Szychowski

Gmiński

2019

Neurochem Res

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The products of elastin degradation, namely elastin-derived peptides (EDPs), are detectable in the cerebrospinal fluid of healthy individuals and in patients after ischemic stroke, and their number increases with age. Depending on their concentrations, both nitric oxide (NO) and reactive oxygen species (ROS) take part either in myocardial ischemia reperfusion injury or in neurovascular protection after ischemic stroke. The aim of our study was to determine the impact of VGVAPG peptide on ROS and NO production and expression of endothelial nitric oxide synthase (eNos), inducible nitric oxide synthase (iNos) and neuronal nitric oxide synthase (nNos) in mouse cortical astrocytes in vitro. Primary astrocytes were maintained in DMEM/F12 without phenol red supplemented with 10% fetal bovine serum. The cells were exposed to rising VGVAPG peptide concentrations, and ROS and NO production was measured. After 6 h (for mRNA) and 24 (for the protein) of exposure to 10 nM and 1 µM of the peptide, expression of nNos, iNos and eNos was measured. Moreover, the Glb1 siRNA gene knockdown method and Pioglitazone, a peroxisome proliferator-activated receptor gamma (Pparγ) agonist, were applied. Our study shows that the VGVAPG peptide decreased eNos, iNos and nNos mRNA and protein expression in mouse astrocytes in vitro. The VGVAPG peptide also decreased NO production while increasing ROS production in the cells. Furthermore, silencing of the Glb1 gene reversed all effects caused by the VGVAPG peptide. However, due to the lack of sufficient data explaining the molecular mechanism of action of the VGVAPG peptide in the nervous system, more studies in this area are necessary.

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Section: Discussionmentioning

confidence: 99%

The VGVAPG Peptide Regulates the Production of Nitric Oxide Synthases and Reactive Oxygen Species in Mouse Astrocyte Cells In Vitro

Szychowski

Gmiński

2019

Neurochem Res

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“…For example, elastin-derived peptides can activate the mitogen-activated protein kinase (MAPK) pathway in VSMCs to stimulate proliferation ( 25 ). Further, endothelial nitric oxide synthase (eNOS) produced by endothelial cells can be activated by tropoelastin, leading to the subsequent release of nitric oxide (NO), a molecule important for its vascular protective functions ( 26 ).…”

Section: Ecm Components Structure and Functionmentioning

confidence: 99%

TRAIL signals, extracellular matrix and vessel remodelling

2020

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The extracellular matrix (ECM) is an essential part of the vasculature, not only providing structural support to the blood vessel wall, but also in its ability to interact with cells to regulate cell phenotype and function including proliferation, migration, differentiation and death; processes important in vascular remodelling. Increasing evidence implicates TNF-related apoptosis-inducing ligand (TRAIL) signalling in the modulation of vascular cell function and remodelling under normal and pathological conditions such as in atherosclerosis. TRAIL can also stimulate synthesis of multiple ECM components within blood vessels. This review explores the relationship between TRAIL signals, the ECM, and its implications in vessel remodelling in cardiovascular disease.

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“…Similar observations were obtained from an ex vivo study, where the treatment of both explanted WT and TSP1 −/− muscle biopsies in collagen matrices with DETA-NONOate (10 mM) caused enhanced relative vascular outgrowth in the later biopsies owing to the inhibited expression of TSP-1. However, the binding peptides to CD36, CD47 or heparin sulfate proteoglycans derived from TSP-1 inhibited this outgrowth, but NoC1 enhanced the vascular outgrowth The exogenous κ-elastin enhances the mRNA expression of eNOS in the ECs [73], and tropoelastin improves the protein expression for NO production, which is inhibited by L-NAME [74]. The TSP-1-mediated inhibition of NO synthesis and downstream effects is through two main mechanisms: (1) The high concentrations of TSP-1 and its peptide mimetics, ABT-510, via interaction with CD-36, inhibit the translocation of myristate to the cytoplasm, thus inhibit the membrane translocation of the Src responsible the activation of eNOS and generation of NO [68,70].…”

Section: Influence Of the Ecm And No On Tumour Angiogenesismentioning

confidence: 99%

The role of extracellular matrix in tumour angiogenesis: the throne has NOx servants

Alsharabasy

Glynn

Pandit

2020

Biochemical Society Transactions

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The extracellular matrix (ECM) dynamics in tumour tissue are deregulated compared to the ECM in healthy tissue along with disorganized architecture and irregular behaviour of the residing cells. Nitric oxide (NO) as a pleiotropic molecule exerts different effects on the components of the ECM driving or inhibiting augmented angiogenesis and tumour progression and tumour cell proliferation and metastasis. These effects rely on the concentration of NO within the tumour tissue, the nature of the surrounding microenvironment and the sensitivity of resident cells to NO. In this review article, we summarize the recent findings on the correlation between the levels of NO and the ECM components towards the modulation of tumour angiogenesis in different types of cancers. These are discussed principally in the context of how NO modulates the expression of ECM proteins resulting in either the promotion or inhibition of tumour growth via tumour angiogenesis. Furthermore, the regulatory effects of individual ECM components on the expression of the NO synthase enzymes and NO production were reviewed. These findings support the current efforts for developing effective therapeutics for cancers.

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Tropoelastin Enhances Nitric Oxide Production by Endothelial Cells

Cited by 10 publications

References 34 publications

The VGVAPG Peptide Regulates the Production of Nitric Oxide Synthases and Reactive Oxygen Species in Mouse Astrocyte Cells In Vitro

The VGVAPG Peptide Regulates the Production of Nitric Oxide Synthases and Reactive Oxygen Species in Mouse Astrocyte Cells In Vitro

TRAIL signals, extracellular matrix and vessel remodelling

The role of extracellular matrix in tumour angiogenesis: the throne has NOx servants

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