Abstract
The current knowledge of the development and progression of atherosclerotic lesions is largely owed to experimental studies carried out in animals fed a high cholesterol diet. Only a few studies have addressed the atherogenic effects of other important exogenous risk factor, namely cigarette smoking. The results of our research into the effects of cigarette smoking on the fetal arterial wall have demonstrated that the first reactive event is a severe alteration of the architecture of the tunica media, forming perpendicularly oriented columns of smooth muscle cells (SMCs), infiltrating the intima. These histopathological alterations go hand in hand with a marked change in the biological homeostasis of the SMCs. Our molecular biology research has shown that the first reaction of these cells to the nicotine is an intense activation of the c-fos proto-oncogene, followed by the transformation of the SMCs to “myofibroblasts”, characterized by the presence of β-actin and acquisition of both synthetic and ameboid activity. If the harmful effects of passive smoke persist, the myofibroblasts start to proliferate, as demonstrated by positivity of the PCNA, together with the onset of chromosomal alterations. These peculiar changes of the tunica media are the prerequisites for lipid accumulation that thereafter overwhelm the myofibroblast reaction.
Keywords: Atherosclerosis, smooth muscle cells, myofibroblasts, cigarette smoke
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