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Altered cellular responses to serum mitogens, including platelet‐derived growth factor, in cultured smooth muscle cells derived from arteries of patients with moyamoya disease
Author(s) -
Aoyagi Masaru,
Fukai Naomi,
Sakamoto Hiroshi,
Shinkai Tadashi,
Matsushima Yoshiharu,
Yamamoto Mari,
Yamamoto Kiyotaka
Publication year - 1991
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041470202
Subject(s) - moyamoya disease , platelet derived growth factor receptor , growth factor , platelet derived growth factor , medicine , pathogenesis , endocrinology , dna synthesis , epidermal growth factor , biology , pathology , in vitro , biochemistry , receptor
Progressive stenosis or occlusion of bi ateral internal carotid arteries by fibrocellular intimal thickening results in cerebral ischemia in moyamoya disease. The etiology is unknown. We examined cultured arterial smooth muscle cells (SMC) from scalp arteries of five patients with moyamoya disease. In this study we investigated the responsiveness of the cells in culture to serum mitogens including platelet‐derived growth factor (PDGF), a major mitogen of SMC, and compared the response to that of cells derived from age‐matched control patients. SMC from patients with moyamoya disease proliferated less rapidly in a medium with 15% serum than did control SMC and responded poorly to the addition of PDGF to 5% serum. PDGF alone did not stimulate SMC in a quiescent state to initiate DNA synthesis in moyamoya disease, without serum factors other than bovine serum albumin, though it significantly stimulated the controls. Simultaneous additions of epidermal growth factor, insulin‐like growth factor‐I, and PDGF stimulated initiation of DNA synthesis in cells from moyamoya disease, but not as much as PDGF alone did in the controls. Although direct correlations with the pathogenesis of the disease remain to be clarified, the results indicate altered interrelations between serum factors and the cellular responses in vessels of moyamoya disease.