TABLE 1.
Comparative analysis of Tat and bFGF angiogenic effectsa
| Biological effect | Effect exhibited in response to:
|
|
|---|---|---|
| Tat | bFGF | |
| EC invasion | No | Yes |
| IC-EC invasion | Yes | Yesb |
| KSC invasion | Yes | Yesc |
| EC migration | No | Yes |
| IC-EC migration | Yes | Yesb |
| KSC migration | Yes | Yesc |
| EC growth | No | Yes |
| IC-EC growth | Yes | Yesd |
| KSC growth | Yes | Yesc |
Human umbilical vein endothelial cells were cultured for 5 days in the absence (endothelial cells [EC]) or in the presence of human recombinant IL- 1β, TNF-α, and IFN-γ (endothelial cells activated by inflammatory cytokines [IC-EC]) combined together at 5, 0.5, and 0.1 ng/ml, respectively. KSC were obtained from AIDS-KS lesions, cultured, and characterized as previously reported (130, 154). Data from references 2, 15, 17, 52-54, and 59-61.
IC-EC show enhanced invasion and migration in response to bFGF compared to EC. This is probably due to a synergy between bFGF and inflammatory cytokines in the induction of metalloproteases (80).
The effect of bFGF on KSC invasion, migration, and growth is less evident than that exerted on EC. This is probably due to autocrine bFGF production by KSC (51, 54, 55).
Exogenous bFGF promotes IC-EC growth to a lesser extent than EC. This is in agreement with IL-1's capability of down-regulating the expression of high-affinity bFGF receptors in the endothelium (44).