dc.creator | Ballesteros Martínez, Constanza | es |
dc.creator | Rodrigues Díez, Raquel | es |
dc.creator | Beltrán Romero, Luis Matías | es |
dc.creator | Moreno Carriles, Rosa | es |
dc.creator | Martínez Martínez, Ernesto | es |
dc.creator | González Amor, María | es |
dc.creator | Briones, Ana M. | es |
dc.date.accessioned | 2022-10-17T16:12:05Z | |
dc.date.available | 2022-10-17T16:12:05Z | |
dc.date.issued | 2022 | |
dc.identifier.citation | Ballesteros Martínez, C., Rodrigues Díez, R., Beltrán Romero, L.M., Moreno Carriles, R., Martínez Martínez, E., González Amor, M. y Briones, A.M. (2022). Microsomal prostaglandin E synthase-1 is involved in the metabolic and cardiovascular alterations associated with obesity. BRITISH JOURNAL OF PHARMACOLOGY, 179 (11), 2733-2753. https://doi.org/10.1111/bph.15776. | |
dc.identifier.issn | 0007-1188 | es |
dc.identifier.issn | 1476-5381 | es |
dc.identifier.uri | https://hdl.handle.net/11441/137971 | |
dc.description.abstract | Background and Purpose: Microsomal prostaglandin E synthase-1 (mPGES-1) is an
inducible isomerase responsible for prostaglandin E2 production in inflammatory con ditions. We evaluated the role of mPGES-1 in the development and the metabolic
and cardiovascular alterations of obesity.
Experimental Approach: mPGES-1+/+ and mPGES-1 / mice were fed with normal
or high fat diet (HFD, 60% fat). The glycaemic and lipid profile was evaluated by glu cose and insulin tolerance tests and colorimetric assays. Vascular function, structure
and mechanics were assessed by myography. Histological studies, q-RT-PCR, and
western blot analyses were performed in adipose tissue depots and cardiovascular
tissues. Gene expression in abdominal fat and perivascular adipose tissue (PVAT)
from patients was correlated with vascular damage.
Key Results: Male mPGES-1 / mice fed with HFD were protected against body
weight gain and showed reduced adiposity, better glucose tolerance and insulin sensi tivity, lipid levels and less white adipose tissue and PVAT inflammation and fibrosis,
compared with mPGES-1+/+ mice. mPGES-1 knockdown prevented cardiomyocyte
hypertrophy, cardiac fibrosis, endothelial dysfunction, aortic insulin resistance, and
vascular inflammation and remodelling, induced by HFD. Obesity-induced weight
gain and endothelial dysfunction of resistance arteries were ameliorated in female
mPGES-1 / mice. In humans, we found a positive correlation between mPGES-1
expression in abdominal fat and vascular remodelling, vessel stiffness, and systolic
blood pressure. In human PVAT, there was a positive correlation between mPGES-1
expression and inflammatory markers.
Conclusions and Implications: mPGES-1 inhibition might be a novel therapeutic
approach to the management of obesity and the associated cardiovascular and meta bolic alterations. | es |
dc.format | application/pdf | es |
dc.format.extent | 21 | es |
dc.language.iso | eng | es |
dc.publisher | Wiley-Blackwell | es |
dc.relation.ispartof | BRITISH JOURNAL OF PHARMACOLOGY, 179 (11), 2733-2753. | |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject | Adipose tissue alterations | es |
dc.subject | Inflammation | es |
dc.subject | MPGES-1 | es |
dc.subject | Obesity | es |
dc.subject | Vascular function and remodelling | es |
dc.title | Microsomal prostaglandin E synthase-1 is involved in the metabolic and cardiovascular alterations associated with obesity | es |
dc.type | info:eu-repo/semantics/article | es |
dcterms.identifier | https://ror.org/03yxnpp24 | |
dc.type.version | info:eu-repo/semantics/publishedVersion | es |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | es |
dc.contributor.affiliation | Universidad de Sevilla. Departamento de Medicina | es |
dc.relation.publisherversion | https://bpspubs.onlinelibrary.wiley.com/doi/10.1111/bph.15776 | es |
dc.identifier.doi | 10.1111/bph.15776 | es |
dc.journaltitle | BRITISH JOURNAL OF PHARMACOLOGY | es |
dc.publication.volumen | 179 | es |
dc.publication.issue | 11 | es |
dc.publication.initialPage | 2733 | es |
dc.publication.endPage | 2753 | es |