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Abstract Title:

Mercury exposure induces proinflammatory enzymes in vascular fibroblasts.

Abstract Source:

Clin Investig Arterioscler. 2017 Sep 18. Epub 2017 Sep 18. PMID: 28935286

Abstract Author(s):

Alberto Millán Longo, Óscar Montero Saiz, Claudia Sarró Fuente, Andrea Aguado Martínez, Mercedes Salaices Sánchez

Article Affiliation:

Alberto Millán Longo

Abstract:

INTRODUCTION: Previous studies show that mercury exposure increases cardiovascular risk, although the underlying cellular mechanisms have still not been fully studied. The aim of this project is to study, in vascular fibroblasts (VF), the effect of HgCl2 exposure on the expression of enzymes involved in the synthesis of prostanoids and reactive oxygen species (ROS). These molecules have been shown to participate in the inflammatory response associated with cardiovascular diseases.

MATERIAL AND METHODS: Adventitial VF cultures of Sprague-Dawley rat aortas, shown to beα-actin negative by immunofluorescence, were exposed to HgCl2 (0.05-5μg/mL) for 48h. mRNA and protein levels of cyclooxygenase-2 (COX-2), microsomal prostaglandin E synthase 1 (mPGES-1), thromboxane A2 synthase (TXAS), NADPH oxidase 1 (NOX-1), and 4 (NOX-4) where analyzed using qRT-PCR and westernblot, respectively. NOX activity was determined by chemiluminescence.

RESULTS: HgCl2 exposure increased COX-2, mPGES-1, TXAS, and NOX-1 expression and NOX activity, and decreased NOX-4 expression. The increase in NOX-1 and COX-2 expression was abolished by the treatment with inhibitors of COX-2 (10μM celecoxib) and NOX (300μM apocynin, 0.5μM ML-171).

CONCLUSIONS: 1) HgCl2 increases the expression of pro-inflammatory enzymes involved in ROS and prostanoid synthesis in VF. 2) There is a reciprocal regulation between COX-2 and NOX-1 pathways. 3) These effects can contribute to explain the increase in cardiovascular risk associated to mercury.

Study Type : In Vitro Study

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