Cell proliferation in normal and atherosclerotic human aorta: proliferative splash in lipid-rich lesions

Quantitative analysis of the expression of caspase 3 and caspase 9 in different types of atherosclerotic lesions in the human aorta

“…The observation of changes in the level of CASP9 expression reported in the present study is in good coincidence with the data on "bellshaped" splash in cellularity during the progression of atherosclerosis, reported by us earlier (Orekhov et al, 1998). Earlier we reported that the number of resident and inflammatory cells as well as proliferative activity is dramatically increased in fatty streaks, followed by the significant fall of these parameters in fibrous plaques (Bobryshev et al, 2011;Orekhov et al, 1998Orekhov et al, , 2010.…”

“…Earlier we reported that the number of resident and inflammatory cells as well as proliferative activity is dramatically increased in fatty streaks, followed by the significant fall of these parameters in fibrous plaques (Bobryshev et al, 2011;Orekhov et al, 1998Orekhov et al, , 2010. The fall in both CASP3 and CASP9 expressions in advanced atherosclerotic plaques may be associated with continued domination of necrotic processes, especially in zones, adjusted to the lipid/necrotic core.…”

Atherosclerosis in APOE*3-Leiden Transgenic Mice

“…13 So far, few human data on DNA synthesis during the entire process of atherogenesis are available. 14 Orekhov et al 14 report peak levels of DNA synthesis in lipid-rich lesions, whereas DNA synthesis in fibrous lesions is much lower. The majority of data on DNA synthesis in human atherosclerosis are confined to advanced lesions only.…”

“…They show low levels of DNA synthesis (0% to 2%), [15][16][17][18] but this level is significantly higher than in the nondiseased arterial wall. 14,15,18,19 One study on DNA synthesis in early fatty-streak lesions also reports low values of DNA synthesis (0% to 2%). 20 DNA synthesis in these human lesions is confined primarily to either the macrophage-derived foam cell 15,17,18 or the VSMC.…”

Macrophage Proliferation in Atherosclerosis

“…In fact, cells in human diffuse intimal thickenings have been shown to express proliferation markers. 16 Additional unanswered questions are to what degree the macrophage proliferation actually contributes to lesion progression rather than just replenishment of the macrophage population and to what degree the scavenger receptor status regulates the proliferation. This is underscored by the controversy that exists as to whether the Msr1 plays a role in lesion development as there has been contradictory evidence that knockout or overexpression of the Msr1 affects lesion area and composition in several different mouse models.…”