The Expression of Lipoprotein Receptors Is Increased in the Infarcted Area After Myocardial Infarction Induced in Rats With Cardiac Dysfunction

dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorLIMA, Aline D. de
dc.contributor.authorGUIDO, Maria C.
dc.contributor.authorTAVARES, Elaine R.
dc.contributor.authorCARVALHO, Priscila O.
dc.contributor.authorMARQUES, Alyne F.
dc.contributor.authorMELO, Marcelo D. T. de
dc.contributor.authorSALEMI, Vera M. C.
dc.contributor.authorKALIL-FILHO, Roberto
dc.contributor.authorMARANHAO, Raul C.
dc.date.accessioned2018-05-08T14:30:55Z
dc.date.available2018-05-08T14:30:55Z
dc.date.issued2018
dc.description.abstractLeft ventricular (LV) remodeling after myocardial infarction constitutes the structural basis for ventricular dysfunction and heart failure. The characterization underlying the expression of lipoprotein receptors in cardiac dysfunction is scarcely explored. The aim of this study was to analyze the status of lipoprotein receptors on the infarcted and noninfarcted areas of LV and to verify whether nano particles that mimic the lipid structure of low-density lipoprotein (LDL) and have the ability to bind to LDL receptors (LDE) are taken up more avidly by the noninfarcted LV. 13 male Wistar rats with left coronary artery ligation (myocardial infarction [MI]) and 12 animals with SHAM operation (SHAM) were used in this study. 6 weeks after the procedure, the quantification of low-density lipoprotein receptor (LDLR), LDL receptor-related protein 1 (LRP1), scavenger receptor-class B type I (SR-BI) lipoprotein receptors, and PCNA proliferation marker, and tissue uptake of radioactively labeled LDE were performed. Immunohistochemistry and Western blot analysis showed that LDLR, LRP1, SR-BI, and PCNA, expression in infarcted area of MI was remarkably higher than SHAM and noninfarcted subendocardial (SEN) and interstitial (INT) areas. In addition, in SEN noninfarcted area of MI, the presence of LDLR was about threefold higher than in SHAM SEN and INT noninfarcted areas. The LDE uptake of noninfarcted LV of MI group was about 30% greater than that of SHAM group. In conclusion, these findings regarding the status of lipoprotein receptors after MI induction could help to establish mechanisms on myocardial repairing. In conclusion, infarcted rats with LV dysfunction showed increased expression of lipoprotein receptors mainly in the infarcted area.
dc.description.indexMEDLINE
dc.description.sponsorshipState of Sao Paulo Research Support Foundation (FAPESP, Sao Paulo, Brazil) [2014/03742-0]
dc.description.sponsorshipNational Council for Scientific and Technological Development (CNPq, Brasilia, Brazil)
dc.identifier.citationLIPIDS, v.53, n.2, p.177-187, 2018
dc.identifier.doi10.1002/lipd.12014
dc.identifier.eissn1558-9307
dc.identifier.issn0024-4201
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/26278
dc.language.isoeng
dc.publisherWILEY
dc.relation.ispartofLipids
dc.rightsrestrictedAccess
dc.rights.holderCopyright WILEY
dc.subjectCoronary artery disease
dc.subjectHeart lipid metabolism
dc.subjectLipoprotein receptors
dc.subject.otherlow-density-lipoprotein
dc.subject.otherpostmenopausal women
dc.subject.otherreplacement therapy
dc.subject.othera-i
dc.subject.othercontrolled-trial
dc.subject.otherstable-isotope
dc.subject.otherestrogen
dc.subject.othermetabolism
dc.subject.otherb-48
dc.subject.wosBiochemistry & Molecular Biology
dc.subject.wosNutrition & Dietetics
dc.titleThe Expression of Lipoprotein Receptors Is Increased in the Infarcted Area After Myocardial Infarction Induced in Rats With Cardiac Dysfunction
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.citation.scopus5
hcfmusp.contributor.author-fmusphcALINE DERISIO DE LIMA
hcfmusp.contributor.author-fmusphcMARIA CAROLINA GUIDO
hcfmusp.contributor.author-fmusphcELAINE RUFO TAVARES
hcfmusp.contributor.author-fmusphcPRISCILA OLIVEIRA DE CARVALHO
hcfmusp.contributor.author-fmusphcALYNE FRANCA MARQUES
hcfmusp.contributor.author-fmusphcMARCELO DANTAS TAVARES DE MELO
hcfmusp.contributor.author-fmusphcVERA MARIA CURY SALEMI
hcfmusp.contributor.author-fmusphcROBERTO KALIL FILHO
hcfmusp.contributor.author-fmusphcRAUL CAVALCANTE MARANHAO
hcfmusp.description.beginpage177
hcfmusp.description.endpage187
hcfmusp.description.issue2
hcfmusp.description.volume53
hcfmusp.origemWOS
hcfmusp.origem.pubmed29394450
hcfmusp.origem.scopus2-s2.0-85041288849
hcfmusp.origem.wosWOS:000428450300004
hcfmusp.publisher.cityHOBOKEN
hcfmusp.publisher.countryUSA
hcfmusp.relation.referenceAbbey M, 1999, MATURITAS, V33, P259, DOI 10.1016/S0378-5122(99)00054-7
hcfmusp.relation.referenceAnderson GL, 2004, JAMA-J AM MED ASSOC, V291, P1701
hcfmusp.relation.referenceCampos H, 1997, J CLIN ENDOCR METAB, V82, P3955, DOI 10.1210/jc.82.12.3955
hcfmusp.relation.referenceChan DC, 2015, CLIN SCI, V128, P379, DOI 10.1042/CS20140559
hcfmusp.relation.referenceCOBELLI C, 1987, AM J PHYSIOL, V253, pE551
hcfmusp.relation.referenceCrook D, 1998, CONTRACEPTION, V57, P189, DOI 10.1016/S0010-7824(98)00018-3
hcfmusp.relation.referenceDuvillard L, 2010, J CLIN ENDOCR METAB, V95, P2140, DOI 10.1210/jc.2009-2480
hcfmusp.relation.referenceHodis HN, 2001, ANN INTERN MED, V135, P939, DOI 10.7326/0003-4819-135-11-200112040-00005
hcfmusp.relation.referenceHodis HN, 2016, NEW ENGL J MED, V374, P1221, DOI 10.1056/NEJMoa1505241
hcfmusp.relation.referenceHussain Y, 2015, ARTERIOSCL THROM VAS, V35, P213, DOI 10.1161/ATVBAHA.114.304326
hcfmusp.relation.referenceKarjalainen A, 2000, ARTERIOSCL THROM VAS, V20, P1101, DOI 10.1161/01.ATV.20.4.1101
hcfmusp.relation.referenceKUSHWAHA RS, 1977, ANN INTERN MED, V87, P517, DOI 10.7326/0003-4819-87-5-517
hcfmusp.relation.referenceLamon-Fava S, 2006, ARTERIOSCL THROM VAS, V26, P385, DOI 10.1161/01.ATV.0000199248.53590.e1
hcfmusp.relation.referenceLamon-Fava S, 2003, METABOLISM, V52, P1330, DOI 10.1016/S0026-0495(03)00276-2
hcfmusp.relation.referenceLamon-Fava S, 2008, ARTERIOSCL THROM VAS, V28, P1672, DOI 10.1161/ATVBAHA.108.164541
hcfmusp.relation.referenceLamon-Fava S, 2007, J LIPID RES, V48, P1746, DOI 10.1194/jlr.M700067-JLR200
hcfmusp.relation.referenceLamon-Faval S, 2004, J LIPID RES, V45, P106, DOI 10.1194/jlr.M300179-JLR200
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