Cultured cells derived from Kaposi sarcoma (KS) lesions in HIV-seropos
itive AIDS patients have been injected subcutaneously in nude mice and
purported to induce cell growth and transformation, vascular hyperper
meability and angiogenic features analogous to KS. We re-examined this
rodent model for KS and extended our studies to include similarly man
ipulated human non-KS endothelial cells (EC). We also assessed the tum
origenicity of RSE-1, a transformed cell line derived from rat liver s
inusoidal EC, in the skin of nude mice and in the liver of Freund's co
mplete adjuvant treated rats. Histologic examination of subcutaneously
injected human AIDS-KS and non-KS EC displayed transient focal lesion
s in various stages of immune cell-mediated rejection. In contrast, RS
E-1, in both skin and liver, displayed cell proliferation and early ne
ovascularization. Vascular hyperpermeability (heightened leakage of in
travascular T1 824 or Evan's blue dye) was not observed in skin sites
injected 12hrs previously with AIDS-KS cells. Of note, the growth of R
SE-1 in nude mouse skin (5-7 days post-injection) and rat liver (21 da
ys post-injection) mimicked the vascular proliferative and morphogenic
features of KS. The insufficiency of current animal models of KS and
the enigma of KS etiology require a renewed search for the factors whi
ch promote the growth of human AIDS-KS and transformed EC both in vitr
o and in vivo.