Intimal cell mass-derived atherosclerotic lesions in the abdominal aorta of hyperlipidemic swine Part 1. Cell of origin, cell divisions and cell losses in first 90 days on diet
| Autor: | Hideshige Imai, Dong Nack Kim, K.T. Lee, J. Schmee, Wilbur A. Thomas |
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| Rok vydání: | 1985 |
| Předmět: |
Male
Programmed cell death Arteriosclerosis Swine Cell of origin Cell Cell Count Hyperlipidemias Stimulation Biology Monocytes Muscle Smooth Vascular Andrology chemistry.chemical_compound medicine Animals Platelet Aorta Abdominal Endothelium Microscopy Cell growth Macrophages Microscopy Electron medicine.anatomical_structure chemistry Vacuoles Immunology Autoradiography Diet Atherogenic Cardiology and Cardiovascular Medicine Thymidine Cell Division Intracellular |
| Zdroj: | Atherosclerosis. 56:169-188 |
| ISSN: | 0021-9150 |
| DOI: | 10.1016/0021-9150(85)90017-6 |
| Popis: | Atherosclerotic lesions may originate and develop in a variety of ways. In this study we are focusing our attention on atherosclerotic lesions arising in normally occurring intimal cell masses (ICM) in the abdominal aortas of hyperlipidemic (HL) swine. Times chosen for study were 0, 14, 49 and 90 days on HL diet; mash-fed swine were used as controls. Total numbers of cells in the ICM of HL and mash swine were similar at 14 and 49 days; by 90 days the number of cells had increased dramatically in the HL swine to 8-fold greater than control values. Changes present at 49 days and thus preceding increase in cell numbers included extensive intracellular lipid accumulation with by count nearly half of the ICM cells involved and elevated tritiated thymidine labeling indices (LI) 4-fold greater than control. Differential cell counts by transmission electron microscopy were made on the ICM lesions in the HL swine at 49 and 90 days. More than 95% of all cells were smooth muscle cells (SMC), with relatively few monocytes being present. Calculations from the LI and total cell counts showed that the entire increase in cell numbers could be accounted for by divisions among the resident SMC in the ICM. Further calculations suggested that cell losses (deaths) from the ICM were minimal. Scanning electron microscopy studies reported elsewhere revealed no loss of endothelial integrity. The results suggest: (1) that the lesions arise by stimulation of the resident SMC in the ICM to hyperplastic activity, (2) that the role of monocytes in the early development of these lesions is minimal if any, (3) that in view of the intact endothelium platelets are not likely to play an important role, (4) that ICM cell death is not a major factor, (5) that the most likely candidate for the cell growth stimulatory role (? mitogen) is some component(s) of the excess lipid that accumulates in the ICM. |
| Databáze: | OpenAIRE |
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