title: Immunohistochemical analysis of platelet-derived growth factor-B expression in myocardial tissues in hypertrophic cardiomyopathy.
abstract: Intimal and/or medial hyperplasia of intramyocardial small vessels is thought to be one of the causes of myocardial ischemia in hypertrophic cardiomyopathy (HCM). However, the pathogenesis of such vascular lesions in HCM is not yet known. To evaluate the pathogenic role of platelet-derived growth factor (PDGF-B) and basic fibroblast growth factor (b-FGF), which have a potential to induce cellular and molecular changes observed in the vessels in HCM, we examined the expression of these molecules and PDGF receptors in cardiac tissues from six patients with HCM and seven controls using immunohistochemistry. The percentage of PDGF-B positive cells in the myocyte population in HCM was significantly higher than that in controls (52.6 +/- 16.2 (mean +/- SD) vs. 21.6 +/- 9.6, p < 0.01). PDGF-B was also observed in vascular regions in HCM (61.1 +/- 25.5% of arterioles) but not in controls. There were no significant differences in the expression of b-FGF and PDGF receptors in the myocyte and non-myocyte populations and the vascular regions between the HCM and control groups. Our study revealed that the expression of PDGF-B protein was up-regulated in HCM, suggesting the contribution of this molecule to the development of intramyocardial vasculopathy.
authors.affiliation: First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
authors.forename: J
authors.initials: J
authors.lastname: Suzuki
authors.forename: S
authors.initials: S
authors.lastname: Baba
authors.forename: I
authors.initials: I
authors.lastname: Ohno
authors.forename: M
authors.initials: M
authors.lastname: Endoh
authors.forename: J
authors.initials: J
authors.lastname: Nawata
authors.forename: S
authors.initials: S
authors.lastname: Miura
authors.forename: Y
authors.initials: Y
authors.lastname: Yamamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Sekiguchi
authors.forename: T
authors.initials: T
authors.lastname: Takita
authors.forename: M
authors.initials: M
authors.lastname: Ogata
authors.forename: K
authors.initials: K
authors.lastname: Tamaki
authors.forename: J
authors.initials: J
authors.lastname: Ikeda
authors.forename: K
authors.initials: K
authors.lastname: Shirato
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000032:analysis; D006328:Cardiac Catheterization; D002312:Cardiomyopathy, Hypertrophic / Q000378:metabolism* / Q000473:pathology; D002452:Cell Count; D003331:Coronary Vessels / Q000378:metabolism / Q000473:pathology; D004452:Echocardiography; D004699:Endocardium / Q000378:metabolism / Q000473:pathology; D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000378:metabolism; D006352:Heart Ventricles / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D020574:Proto-Oncogene Proteins c-sis / Q000378:metabolism*; D017479:Receptors, Platelet-Derived Growth Factor / Q000378:metabolism
chemical_list: D015415:Biomarkers; D020574:Proto-Oncogene Proteins c-sis; D016222:Fibroblast Growth Factor 2; D017479:Receptors, Platelet-Derived Growth Factor