The current state of our knowledge of the control of endothelial growth and the role of endothelial injury in the pathogenesis of atherosclerosis can be summarized as follows: 1. Endothelial cells can be grown in plasma-derived serum in the absence of exogenous growth factors. This is quite different from the growth requirements of most other nontransformed cells. These factors may, however, prolong replicative life span and increase the ability of endothelium to grow at sparse density. The relevance of these phenomena to the control of endothelial growth in vivo is unclear. There is no evidence that exogenous growth factors are required for wound edge regeneration. In view of the relative lack of growth factor requirements, it is intriguing to consider the possibility that the critical control factor for endothelial cell growth is cell contact. 2. Endothelial cell regeneration may be dependent on endothelial cell motility. The nature of this relationship may be important in controlling the ability of the endothelium to regenerate itself under different flow conditions around lesions or in different parts of the vessel tree and in determining the ability of the endothelium to respond to changes in the connective tissue overlying lesions. 3. Endothelial cells in vivo are able to regenerate small areas of denudation extremely rapidly. This process may be sufficiently rapid to permit the endothelium to replace dying cells as they are being lost, resulting in desquamation without denudation. 4. We have little evidence for endothelial denudation either spontaneously or in response to atherosclerosis risk factors until after lesion formation has begun. This does not rule out the possibility that small, repeated, transient episodes of denudation occur and play a role in the initiation of atherosclerotic lesions. It is important, however, to begin considering the role of nondenuding injuries in atherosclerosis. 5. The fact that thrombosis occurs in atherosclerosis implies an eventual breakdown of endothelial integrity. The mechanism of that breakdown remains unknown. 6. Finally, there is the question of interactions between smooth muscle cells and endothelial cells at the level of growth control. This includes the evidence that there is a critical amount of endothelium that must be lost before lesion formation is stimulated and the recent evidence that endothelial cells produce substances able to regulate growth of smooth muscle cells.

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We have reconstituted high viscosity networks of actin filaments and microtubules from purified actin, tubulin, and MAPs. MAP-2 can effectively cross-link actin filaments and microtubules, presumably because a low affinity actin binding site is available even when it is bound tightly to microtubules. Phosphorylation of MAP-2 inhibits cross-linking of actin filaments and microtubules. Tau is not an effective cross-linker of actin and microtubules even though it can interact with each polymer individually.