000149098 001__ 149098
000149098 005__ 20250127144949.0
000149098 0247_ $$2doi$$a10.1093/hmg/ddt042
000149098 0248_ $$2sideral$$a81855
000149098 037__ $$aART-2013-81855
000149098 041__ $$aeng
000149098 100__ $$aRodríguez-Calvo, R.
000149098 245__ $$aOver-expression of neuron-derived orphan receptor-1 (NOR-1) exacerbates neointimal hyperplasia after vascular injury
000149098 260__ $$c2013
000149098 5060_ $$aAccess copy available to the general public$$fUnrestricted
000149098 5203_ $$aWe have previously shown that NOR-1 (NR4A3) modulates the proliferation and survival of vascular cells in culture. However, in genetically modified animal models, somewhat conflicting results have been reported concerning the involvement of NOR-1 in neointimal formation after vascular injury. The aim of this study was to generate a transgenic mouse model over-expressing NOR-1 in smooth muscle cells (SMCs) and assess the consequence of a gain of function of this receptor on intimal hyperplasia after vascular injury. The transgene construct (SM22-NOR1) was prepared by ligating the full-length human NOR-1 cDNA (hNOR-1) and a mouse SM22a minimal promoter able to drive NOR-1 expression to SMC. Two founders were generated and two stable transgenic mouse lines (TgNOR-1) were established by backcrossing the transgene-carrying founders with C57BL/6J mice. Real-time PCR and immunohistochemistry confirmed that hNOR-1 was mainly targeted to vascular beds such as aorta and carotid arteries, and was similar in both transgenic lines. Vascular SMC from transgenic animals exhibit increased NOR-1 transcriptional activity (assessed by electrophoretic mobility shift assay and luciferase assays), increased mitogenic activity (deter- mined by [3H]-thymidine incorporation; 1.58-fold induction, P < 0.001) and increased expression of embryonic smooth muscle myosin heavy chain (SMemb) than wild-type cells from control littermates. Using the carotid artery ligation model, we show that neointima formation was increased in transgenic versus wild-type mice (2.36-fold induction, P < 0.01). Our in vivo data support a role for NOR-1 in VSMC proliferation and vascular remodelling. This NOR-1 transgenic mouse could be a useful model to study fibroproliferative vascular diseases.
000149098 536__ $$9info:eu-repo/grantAgreement/ES/ISCIII/RD12-0042-0053$$9info:eu-repo/grantAgreement/ES/MICINN/SAF2009-11949$$9info:eu-repo/grantAgreement/ES/MICINN/SAF2012-40127$$9info:eu-repo/grantAgreement/ES/MINECO/PI12-01952
000149098 540__ $$9info:eu-repo/semantics/openAccess$$aAll rights reserved$$uhttp://www.europeana.eu/rights/rr-f/
000149098 590__ $$a6.677$$b2013
000149098 591__ $$aGENETICS & HEREDITY$$b16 / 164 = 0.098$$c2013$$dQ1$$eT1
000149098 591__ $$aBIOCHEMISTRY & MOLECULAR BIOLOGY$$b32 / 290 = 0.11$$c2013$$dQ1$$eT1
000149098 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/acceptedVersion
000149098 700__ $$aGuadall, A.
000149098 700__ $$aCalvayrac, O.
000149098 700__ $$0(orcid)0000-0002-0108-1004$$aNavarro, M. A.$$uUniversidad de Zaragoza
000149098 700__ $$aAlonso, J.
000149098 700__ $$aFerrán, B.
000149098 700__ $$aDe Diego, A.
000149098 700__ $$0(orcid)0000-0003-2014-2869$$aMuniesa, P.$$uUniversidad de Zaragoza
000149098 700__ $$0(orcid)0000-0002-8251-8457$$aOsada, J.$$uUniversidad de Zaragoza
000149098 700__ $$aRodríguez, C.
000149098 700__ $$aMartínez-González, J.
000149098 7102_ $$11001$$2025$$aUniversidad de Zaragoza$$bDpto. Anatom.,Embri.Genét.Ani.$$cÁrea Anatom.Anatom.Patológ.Com
000149098 7102_ $$11002$$2060$$aUniversidad de Zaragoza$$bDpto. Bioq.Biolog.Mol. Celular$$cÁrea Bioquímica y Biolog.Mole.
000149098 773__ $$g22, 10 (2013), 1949-1959$$pHum. mol. genet.$$tHUMAN MOLECULAR GENETICS$$x0964-6906
000149098 8564_ $$s833490$$uhttps://zaguan.unizar.es/record/149098/files/texto_completo.pdf$$yPostprint
000149098 8564_ $$s804811$$uhttps://zaguan.unizar.es/record/149098/files/texto_completo.jpg?subformat=icon$$xicon$$yPostprint
000149098 909CO $$ooai:zaguan.unizar.es:149098$$particulos$$pdriver
000149098 951__ $$a2025-01-27-14:45:26
000149098 980__ $$aARTICLE