Antiangiogenetic Effects Research Articles

Inhibition of inflammatory angiogenesis in rats by loco-regional administration of hydrocortisone and protamine.

We have studied the antiangiogenetic effects of hydrocortisone and protamine given intra-arterially. The cornea of male, Sprague-Dawley rats were cauterized with silver nitrate. The following treatments were given: 30 micrograms hydrocortisone topical (t.p.), b.i.d., 50 mg/kg/day intraperitoneally (i.p.) or intra-arterially (i.a.), 10 mg/kg/day protamine i.p. or i.a. Saline was administered to the control groups. In separate experiments we also evaluated the anti-inflammatory effects of hydrocortisone, i.p., on the cauterized corneas. Five days after cauterization, the animals were killed, exsanguinated and India ink was injected to show the network of neovessels. The percentage area of the cornea covered by neovessels was measured morphometrically and evaluated statistically. Hydrocortisone t.p. (-84%), i.a. (-60%) and protamine i.a. (-44%) significantly inhibited angiogenesis in the cauterized cornea. Either drugs, i.p., had any antiangiogenetic effects, but hydrocortisone significantly reduced cell infiltration of the corneas. The results suggest that locoregional administration of antiangiogenetic drugs might be clinically useful.

Interferons: Antiangiogenesis Agents (A Reasonable Theory)

Antiviral and immunomodulatory effects of interferons (IFNs) are well‐known. This communication lists arguments for explicit antiangiogenetic effects exerted by interferons. There is strong likelihood that IFNs α, β and γ inhibit the int family of genes whose gene product proteins are the acidic and basic fibroblast growth factors. Some of these growth factors promote the growth of vascular endothelial cells. IFN‐α inhibits basic, and IFN‐γ inhibits acidic fibroblast growth factors. Inhibition of Kaposi sarcoma cell growth is not due to immunological reconstitution of the host. As IFN‐α induces clinical remissions but IFN‐γ does not, basic and not acidic fibroblast growth factor should be implied as one of the proliferation‐inducing factors of Kaposi sarcoma cells. lFNs may interfere with the growth promotional activity of the human immunodeficiency virus Tat protein on Kaposi sarcoma cells. The proliferation of certain melanoma cell populations requires fibroblast growth factors. If this mechanism is mediated through amplified int genes, IFNs may be active clinically in this subset of melanomas. Some breast carcinoma cells induce neovascularization and metastasize. If this activity is mediated through amplified int genes. IFNs may be active clinically in this subset of breast carcinomas.