Redox regulation of c-Ha-ras and osteopontin signaling in vascular smooth muscle cells: implications in chemical atherogenesis.
Reduction/oxidation (redox) reactions play a central role in the regulation of vascular cell functions. Recent studies in this laboratory have identified c-Ha-ras and osteopontin genes as critical molecular targets during oxidant-induced atherogenesis. This review focuses on the deregulation of gene transcription by redox-activated trans-acting factors after benzo(a)pyrene challenge and the modulation of extracellular matrix signaling in vascular smooth muscle cells by allylamine-induced oxidative injury. The induction of atherogenic vascular smooth muscle cell phenotypes by chemical injury exhibits remarkable parallels with those seen in other forms of atherogenesis.
D000818:Animals; D001161:Arteriosclerosis / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism*; D001483:Base Sequence; D018736:DNA Adducts; D004785:Environmental Pollutants / Q000633:toxicity; D011905:Genes, ras; D006801:Humans; D008969:Molecular Sequence Data; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000502:physiology*; D053495:Osteopontin; D016877:Oxidants / Q000633:toxicity; D010084:Oxidation-Reduction; D012795:Sialoglycoproteins / Q000235:genetics*; D015398:Signal Transduction / Q000235:genetics / Q000502:physiology