mObject. Prominent features of moyamoya disease are intimal thickening
of the cerebral arterial trunks and abundant angiogenesis for collate
ral blood supplies, but its pathogenesis is still unknown. The aim of
this study was to test the possibility that transforming growth factor
-beta(1) (TGF beta(1)) may play a role in the pathogenesis of moyamoya
disease. Methods. The authors used reverse transcription-polymerase c
hain reaction to analyze the expression level of TGF beta(1) in smooth
-muscle cells cultured from the superficial temporal arteries (STAs) a
nd measured the serum level of TGF beta(1) by using enzyme-linked immu
nosorbent assay. Although the STA is not predominantly involved with m
oyamoya disease, it has been used in studies of the pathogenesis of th
is disease. In this report, the STAs from six patients with moyamoya d
isease and four with arteriosclerotic cerebrovascular disease, along w
ith sera from 14 patients with moyamoya disease and 10 normal healthy
volunteers, were studied. The expression of TGF beta(1) was significan
tly higher in cultured smooth-muscle cells derived from the STAs of pa
tients with moyamoya disease than in those derived from the STAs of pa
tients with arteriosclerotic cerebrovascular disease (p < 0.05). The s
erum level of TGF beta(1) was also significantly higher in patients wi
th moyamoya disease than in controls (p < 0.0005). Conclusions. Taking
into account the functional roles of TGF beta(1) in the expression of
connective tissue genes and angiogenesis, these investigators suggest
that TGF beta(1) is associated with the pathogenesis of moyamoya dise
ase, including abundant neovascularization, although their findings do
not necessarily mean that TGF beta(1) is a causative factor in this d
isease.