title: Molecular analysis of arterial stenosis in rat carotids.
abstract: A new model of surgical injury for the induction and development of stenosis in common rat carotids is described. This model differs from balloon angioplasty or vein graft systems currently applied on animals to develop stenosis, since it involves the entire vessel wall layers and mimics the injury occurring during arterial grafts, endarterectomy or organ transplantation. At different times following arterial damage, the pattern of expression of genes already known to be involved in the proliferation, differentiation, and apoptosis of smooth muscle cells (c-myc, Angiotensin II receptor 1, Bcl-2 and Bax alpha), as well as of Rb and Rb2 genes, whose pattern of expression after arterial injury has not yet been reported, was analyzed by semi-quantitative reverse transcription-polymerase chain reaction technique. Histological and histochemical analysis on carotid sections shows the morphological changes which occurred 30 days after surgical injury in the vessel wall. Molecular and histological data demonstrate that this model of surgical injury induces neointimal proliferation in about 30% of rats. In about 70% of the remaining rats, it induces the processes responsible for negative remodelling, namely the significant accumulation of extracellular matrix and fibers and disorganization of arterial tunics. This model is therefore available for further studies on the expression of genes involved in the arterial stenotic process, as well as for testing drugs aimed at limiting this recurrent pathophysiological phenomenon.
authors.affiliation: Institute of Pharmacology and Toxicology, Second University of Naples, Via Constantinopoli, 16, 80138 Naples, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Forte
authors.forename: G
authors.initials: G
authors.lastname: Di Micco
authors.forename: U
authors.initials: U
authors.lastname: Galderisi
authors.forename: F M
authors.initials: FM
authors.lastname: Guarino
authors.forename: M
authors.initials: M
authors.lastname: Cipollaro
authors.forename: M
authors.initials: M
authors.lastname: De Feo
authors.forename: R
authors.initials: R
authors.lastname: Gregorio
authors.forename: M R
authors.initials: MR
authors.lastname: Bianco
authors.forename: C
authors.initials: C
authors.lastname: Vollono
authors.forename: F
authors.initials: F
authors.lastname: Esposito
authors.forename: L
authors.initials: L
authors.lastname: Berrino
authors.forename: F
authors.initials: F
authors.lastname: Angelini
authors.forename: A
authors.initials: A
authors.lastname: Renzulli
authors.forename: M
authors.initials: M
authors.lastname: Cotrufo
authors.forename: F
authors.initials: F
authors.lastname: Rossi
authors.forename: A
authors.initials: A
authors.lastname: Cascino
mesh_terms: D000818:Animals; D017209:Apoptosis; D002339:Carotid Arteries / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D016893:Carotid Stenosis / Q000235:genetics* / Q000473:pathology; D004195:Disease Models, Animal; D005786:Gene Expression Regulation; D016161:Genes, Retinoblastoma; D019254:Genes, bcl-2; D016259:Genes, myc; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D011518:Proto-Oncogene Proteins / Q000235:genetics; D019253:Proto-Oncogene Proteins c-bcl-2; D051381:Rats; D011921:Rats, Inbred WKY; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D051028:bcl-2-Associated X Protein
chemical_list: C494828:Bax protein, rat; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin; D051028:bcl-2-Associated X Protein