Platelet factors and the human vascular wall: variations in growth response between endothelial and medial smooth muscle cells
- PMID: 678311
- DOI: 10.1016/0021-9150(78)90153-3
Platelet factors and the human vascular wall: variations in growth response between endothelial and medial smooth muscle cells
Abstract
In the present investigations, the effects of platelet factors on DNA-synthesis by human arterial and venous smooth muscle and venous endothelial cells were compared. Also studied was the role of such factors in restimulating quiescent endothelial cultures and in endothelial reaction to injury. Aortic smooth muscle cells grown in medium containing 10% human serum prepared from plasma poor in platelets (PPPS) reached 9.7%+/-SE 0.65 labelling index when continuously exposed to [3H] thymidine (1 muCi/ml). When lysate from gel-filtered platelets was added, the index was 19.4% +/- SE 1.13 (P less than 0.01) and in the presence of serum derived from platelet rich plasma (PRPS) it reached 24.6% +/- SE 1.22 (P less than 0.01). Similar results were obtained with smooth muscle cells from umbilical veins. In constrast, platelet factors did not significantly affect DNA-synthesis in endothelial cultures. They reached 25.6% +/- SE 1.97 when grown in medium containing PPPS as compared to 21.9% +/- Se 2.53 (P greater than 0.05), when exposed to PRPS. The ability of sera to stimulate DNA-synthesis in endothelial cultures rendered quiescent by 24 h exposure to medium containing 1.4% serum albumin (labelling index 1.83% +/- SE 0.14) was not affected by platelet factors. Platelet lysates alone were not sufficient to restimulate the quiescent cells (labelling index 3.03% +/- SE 1.06) (P greater than 0.05). Platelet factors did not affect the proliferative response following experimental mechanical injury to endothelial monolayers in vitro. We conclude that while platelet factors are essential for human vascular smooth muscle cells to achieve optimal growth, they are not indispensable for endothelial cell proliferation. It is suggested that these cellular differences in growth requirements may play an important role in human atherogenesis.
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