The role of histidine decarboxylase in the proliferation of vascular smooth muscle cells in culture

• Published in: Japanese Journal of Pharmacology 1999, Vol.79 (suppl.1), p.217-217
• Main Authors: Kobayashi, Fuminori, Fang, Yang-Il, Momose, Kazutaka
• Format: Article
• Language: English
• ISSN: 0021-5198; 1347-3506
• DOI: 10.1016/S0021-5198(19)34882-6

Proliferation of vascular smooth muscle cells (SMCs) is an essential component in pathogenesis of atherosclerosis and restenosis after angioplasty. Recently, we have observed a marked upregulation of histidine decarboxylase (HDC), a histamine-forming enzyme, in proliferating SMCs at the neointima of balloon-injured porcine coronary artery. On the other hand, it is well known that the cultured SMCs are similar in phenotype with the neointimal SMCs. In the present study, we examined the presence and role of HDC in the proliferation of the cultured SMCs from porcine coronary artery. Cultured SMCs were prepared by explant of medial layer of porcine coronary artery. From the immunohistochemical study with the anti-HDC antibody, positive immunostaining of HDC was observed in the perinuclear region and cytoplasm of the cultured cells. In consistent with the previous report, western blot analysis revealed a 53 kD protein immunoreactive for HDC in the cultured cells. These results demonstrated the presence of HDC in the cultured SMCs. Proliferation of cultured SMCs was determined by [^^3 H]-thymidine uptake into the cells. Upon stimulation with platelet-derived growth factor (PDGF; 10 ng/ml), the cultured cells showed 6-fold increase in the uptake of [^^3 H]-thymidine. Alpha-methylhistidine, an inhibitor of HDC, inhibited the PDGF-stimulated [^^3 H]-thymidine uptake into the cells by 45% at maximum. These result suggest the potential role of HDC in the proliferation of cultured SMCs.