High levels of homocysteine inhibit lysyl oxidase (LOX) and downregulate LOX expression in vascular endothelial cells

Raposo, Berta; Rodrı́guez, Cristina; Martínez-González, José; Badimon, Lina

doi:10.1016/j.atherosclerosis.2004.06.015

Cited by 122 publications

(70 citation statements)

References 39 publications

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“…Pancreatitis-associated protein is reported to be related to play a role in inflammatory pancreatitis (43). Lysyl oxidase is an enzyme involved in extracellular matrix maturation (44). Prostaglandin F2α is reported to have the ability to oxidize arachidonate.…”

Section: Discussionmentioning

confidence: 99%

Amelioration of Hypertensive Heart Failure by Amlodipine May Occur via Antioxidative Effects

et al. 2006

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Although recent clinical studies have suggested that long-acting calcium channel blockers (CCBs) have beneficial effects on heart failure, the precise mechanism is unknown. In this study, Dahl salt-sensitive rats fed a high salt diet were treated with the long-acting CCB amlodipine, the low-molecular-weight membrane permeable superoxide dismutase mimetic 4-hydroxy-2,2,6,6-tetramethyl piperidinoxyl (Tempol), or saline from 11 weeks after birth. The cardiac geometry and function, and gene expression profiles were determined at 17 weeks. Dahl salt-sensitive rats fed a high salt diet followed by saline as a non-treatment control (HS group) showed a marked increase in blood pressure and developed concentric hypertrophy at 11 weeks, fol-

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Section: Discussionmentioning

confidence: 99%

Amelioration of Hypertensive Heart Failure by Amlodipine May Occur via Antioxidative Effects

et al. 2006

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“…The construction of luciferase-linked promoter reporter plasmids containing the 22,073/11434 proximal region of the murine lox gene or the 2712/21 proximal region of the human loxl1 gene in pGL2 (Promega, Madison, WI) has already been described (27,28), as has the construction of a luciferase-linked promoter reporter plasmid containing 1,547 bp of 59 flanking sequence from the human lox gene with a pGL3 backbone (29).…”

Section: Luciferase-based Promoter Reporter Assaymentioning

confidence: 99%

Lysyl Oxidase Activity Is Dysregulated during Impaired Alveolarization of Mouse and Human Lungs

Kumarasamy¹,

Schmitt²,

Nave³

et al. 2009

Am J Respir Crit Care Med

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Rationale: Disordered extracellular matrix production is a feature of bronchopulmonary dysplasia (BPD). The basis of this phenomenon is not understood. Objectives: To assess lysyl oxidase expression and activity in the injured developing lungs of newborn mice and of prematurely born infants with BPD or at risk for BPD. Methods: Pulmonary lysyl oxidase and elastin gene and protein expression were assessed in newborn mice breathing 21 or 85% oxygen, in patients who died with BPD or were at risk for BPD, and in control patients. Signaling by transforming growth factor (TGF-b) was preemptively blocked in mice exposed to hyperoxia using TGFb-neutralizing antibodies. Lysyl oxidase promoter activity was assessed using plasmids containing the lox or loxl1 promoters fused upstream of the firefly luciferase gene. Measurements and Main Results: mRNA and protein levels and activity of lysyl oxidases (Lox, LoxL1, LoxL2) were elevated in the oxygeninjured lungs of newborn mice and infants with BPD or at risk for BPD. In oxygen-injured mouse lungs, increased TGF-b signaling drove aberrant lox, but not loxl1 or loxl2, expression. Lox expression was also increased in oxygen-injured fibroblasts and pulmonary artery smooth muscle cells. Conclusions: Lysyl oxidase expression and activity are dysregulated in BPD in injured developing mouse lungs and in prematurely born infants. In developing mouse lungs, aberrant TGF-b signaling dysregulated lysyl oxidase expression. These data support the postulate that excessive stabilization of the extracellular matrix by excessive lysyl oxidase activity might impede the normal matrix remodeling that is required for pulmonary alveolarization and thereby contribute to the pathological pulmonary features of BPD.

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“…HUVECs were transfected using Lipofectin™ (Life Technologies) as previously described (40). Briefly, transfections were carried out with 1 mg/well of the construct pGL3/PTGIS-1963, 0.3 mg/well of pSVb-gal, and 3 ml of Lipofectin™.…”

Section: Transient Transfection Assaysmentioning

confidence: 99%

Retinoic acid induces PGI synthase expression in human endothelial cells

Camacho

Rodrı́guez

Salazar

et al. 2008

Journal of Lipid Research

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Retinoic acid (RA) exhibits anti-inflammatory, anti-tumor, and immuno-modulatory actions, and affects angiogenesis and thrombosis. Arachidonic acid (AA) metabolites are involved in all these processes. We explored the effect of RA on AA metabolism in human umbilical vein endothelial cells (HUVECs). 13-cis -RA increased the release of prostaglandin I 2 (PGI 2) , both spontaneous and thrombin-induced, in terms of 6-oxo-PGF 1a analyzed by enzyme-immunoassay. Coincubation with 13-cis-RA and interleukin-1b resulted in a synergic increase in the release of PGI 2 . Consistently, 13-cis -RA increased the ability of HUVECs to inhibit AA-induced platelet aggregation. 13-cis-RA did not induce cyclooxygenase-isoenzyme expression, determined by immunoblotting, or activity, evaluated by analyzing eicosanoids formed from exogenous labeled AA by HPLC. In contrast, RA induced PGI synthase (PGIS) activity and expression in terms of mRNA and protein determined by real-time PCR and Western blotting, respectively. Results from experiments with several species of RA and with retinoic acid receptor (RAR) and retinoid X receptor (RXR) antagonists showed that the effect of RA on PGIS expression was mediated by RAR. Actinomycin D and cycloheximide both inhibited RA-induced PGIS expression. Furthermore, RA increased PGIS transcriptional activity in transient transfection assays, an effect that was prevented by an RAR antagonist. These results reinforce the concept that RA could be beneficial for patients with cardiovascular risk.-Camacho, M., C. Rodríguez, J. Salazar, J. Martínez-González, J. Ribalta, J-R. Escudero, L. Masana, and L. Vila. Retinoic acid induces PGI synthase expression in human endothelial cells.

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High levels of homocysteine inhibit lysyl oxidase (LOX) and downregulate LOX expression in vascular endothelial cells

Cited by 122 publications

References 39 publications

Amelioration of Hypertensive Heart Failure by Amlodipine May Occur via Antioxidative Effects

Amelioration of Hypertensive Heart Failure by Amlodipine May Occur via Antioxidative Effects

Lysyl Oxidase Activity Is Dysregulated during Impaired Alveolarization of Mouse and Human Lungs

Retinoic acid induces PGI synthase expression in human endothelial cells

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