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Am J Pathol. 2001 May;158(5):1685-94.

Expression of a novel RNA-splicing factor, RA301/Tra2beta, in vascular lesions and its role in smooth muscle cell proliferation.

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  • 1Department of Pathology and Neurosurgery, National Cardiovascular Center, Suita City, Japan. ytukamot@hsp.ncvc.go.jp


RA301/Tra2beta, a sequence-specific RNA-binding protein, was first cloned as a stress molecule in re-oxygenated astrocytes. In human vascular tissues, we have found enhanced RA301/Tra2beta expression in coronary artery with intimal thickening, and atherosclerotic aorta. Balloon injury to the rat carotid artery induced RA301/Tra2beta transcripts followed by expression of the antigen, which was detected in medial and neointimal vascular smooth muscle cells (VSMCs). In cultured VSMCs, hypoxia/re-oxygenation caused induction of RA301/Tra2beta and was accompanied by cell proliferation, both of which were blocked by the addition of either diphenyl iodonium, a NADPH oxidase inhibitor, PD98059, a mitogen-activated protein kinase kinase inhibitor, or antisense oligonucleotide for RA301/Tra2beta. Consistent with a link between RA301/Tra2beta and cell proliferation, platelet-derived growth factor also induced expression of RA301/Tra2beta in cultured VSMCS: These data suggest a possible role for RA301/Tra2beta in the regulation of VSMC proliferation, especially in the setting of hypoxia/re-oxygenation-induced cell stress.

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