Abstract
Basic fibroblast growth factor (bFGF) and human immunodeficiency virus type 1 (HIV-1) Tat protein synergize in inducing angiogenic Kaposi's sarcoma-like lesions in mice. Synergy is due to Tat, which enhances endothelial cell growth and type-IV collagenase expression in response to bFGF mimicking extracellular matrix proteins. The bFGF, extracellular Tat and Tat receptors are present in HIV-1-associated KS, which may explain the higher frequency and aggressiveness of this form compared to classical Kaposi's sarcoma where only bFGF is present.
MeSH terms
-
Acquired Immunodeficiency Syndrome / complications*
-
Acquired Immunodeficiency Syndrome / virology
-
Animals
-
Base Sequence
-
Cell Adhesion
-
Cell Line
-
Collagenases / metabolism
-
Enzyme Activation
-
Extracellular Matrix Proteins / physiology
-
Fibroblast Growth Factor 2 / physiology*
-
Fibronectins / physiology
-
Gene Products, tat / physiology*
-
HIV-1 / physiology*
-
Humans
-
Matrix Metalloproteinase 9
-
Mice
-
Mice, Inbred BALB C
-
Mice, Nude
-
Molecular Mimicry
-
Molecular Sequence Data
-
Palatine Tonsil / pathology
-
Sarcoma, Kaposi / etiology*
-
Sarcoma, Kaposi / pathology
-
Sarcoma, Kaposi / virology
-
Skin / pathology
-
tat Gene Products, Human Immunodeficiency Virus
Substances
-
Extracellular Matrix Proteins
-
Fibronectins
-
Gene Products, tat
-
tat Gene Products, Human Immunodeficiency Virus
-
Fibroblast Growth Factor 2
-
Collagenases
-
Matrix Metalloproteinase 9