title: C-Type natriuretic peptide and natriuretic peptide receptors are expressed by smooth muscle cells in the neointima after percutaneous coronary intervention.
abstract: Understanding restenosis after percutaneous coronary intervention (PCI) remains a challenge. Neointimal proliferation is the main cause of restenosis. C-Type natriuretic peptide (CNP) plays a role in relaxation and growth inhibition of vascular smooth muscle cells (SMCs); the effects depend on the presence of specific natriuretic peptide receptors (NPRs) consisting of NPR-A, NPR-B, and NPR-C. To test the hypothesis that CNP and NPRs may be involved in restenosis, we immunohistochemically studied the expression of CNP and NPRs during the post-PCI healing process; 10 sites after PCI obtained at autopsy and 14 atherectomy specimens obtained from restenotic sites were investigated. Frozen sections were stained with antibodies against CNP, NPRs, SMCs, macrophages, and endothelial cells. Within 2 months after PCI, most neointimal SMCs expressed CNP and NPR-A. The expression of CNP and NPR-A in these neointimal SMCs decreased from 6 months onward. In contrast, NPR-C was strongly expressed in neointimal SMCs from 1 to 9 months after PCI. In atherectomy specimens, most neointimal SMCs showed weak positivity for CNP and NPR-A, but NPR-C was strongly expressed in the neointimal SMCs. These findings strongly suggest that a paracrine and autocrine system of CNP and NPRs may be important in controlling neointimal growth after PCI in humans.
authors.affiliation: Department of Cardiology, Osaka City General Hospital, 2-13-22 Miyakojima-hondori, Osaka 534-0021, Japan. tmnaruko@msic.med.osaka-cu.ac.jp
authors.forename: Takahiko
authors.initials: T
authors.lastname: Naruko
authors.forename: Akira
authors.initials: A
authors.lastname: Itoh
authors.forename: Kazuo
authors.initials: K
authors.lastname: Haze
authors.forename: Shoichi
authors.initials: S
authors.lastname: Ehara
authors.forename: Hiroko
authors.initials: H
authors.lastname: Fukushima
authors.forename: Yoshimi
authors.initials: Y
authors.lastname: Sugama
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Shirai
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Ikura
authors.forename: Masahiko
authors.initials: M
authors.lastname: Ohsawa
authors.forename: Makiko
authors.initials: M
authors.lastname: Ueda
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D017225:Atherectomy, Coronary; D003324:Coronary Artery Disease / Q000378:metabolism / Q000473:pathology / Q000628:therapy; D023903:Coronary Restenosis / Q000209:etiology* / Q000378:metabolism* / Q000473:pathology; D005260:Female; D006162:Guanylate Cyclase / Q000378:metabolism*; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000378:metabolism* / Q000473:pathology; D020098:Natriuretic Peptide, C-Type / Q000378:metabolism*; D017461:Receptors, Atrial Natriuretic Factor / Q000378:metabolism*; D017539:Tunica Intima / Q000378:metabolism / Q000473:pathology; D000099242:Atrial Natriuretic Factor Receptor B
chemical_list: D006162:Guanylate Cyclase; D020098:Natriuretic Peptide, C-Type; D017461:Receptors, Atrial Natriuretic Factor; D000099242:Atrial Natriuretic Factor Receptor B; C091715:atrial natriuretic factor receptor A; C073616:atrial natriuretic factor receptor C