[DESIALATED LOW DENSITY LIPOPROTEINS IN HUMAN BLOOD].

The present article is a review of literature on circulating low-density lipoproteins (LDLP) which can induce accumulation of lipids (mainly, cholesterol), in a SMA(+) cell culture of normal human aortic intima. An attempt was undertaken to resolve the paradox of the absence of both native LDLP influence on intracellular lipid accumulation and modifications of in vitro obtained LDLP in the blood-vascular system. It was showed that atherogenic LDLPs are characterized by a number of changes in carbon, protein and lipid components which can be regarded as multiple modifications of LDLP taking place in human blood plasma. Multiply modified circulating LDLP possess of capacity to interact with various cell membrane receptors differing from B and E receptor, and with proteoglycans. Marked absorption of desiliated LDLPs by the cells simultaneous with a decrease in the degradation of apolipoproteins and cholesterol esters as well as induction of peresterification of free cholesterol leads to intracellular accumulation of esterified cholesterol. Formation of large LDLP-containing complexes especially circulating low-density lipoproteins can stimulate accumulation of lipids by smooth muscle cells of intima. Desiliated LDLPs stimulated cell proliferation and connective tissue matrix synthesis despite cholesterol ester accumulation. In conclusion, the authors of this article found and characterized natural multiply modified LDLPs that can be responsible for the symptoms of atherosclerosis at the cellular level.