Vessels in benign prostatic hyperplasia contain more binding sites for endostatin than vessels in normal prostate tissue.
OBJECTIVE
The angiogenic phenotype is an effect of a net balance of angiogenic and anti-angiogenic factors. Endostatin is one of a group of recently described matrix-derived inhibitors of tumour angiogenesis that have acquired increasing significance for tumour treatment. Endostatin's anti-angiogenic mechanism and the causes of its heterogenic influence on various tissue types have not yet been defined.


METHODS
We investigated the variations in endostatin's binding behaviour to vessels in benign prostatic hyperplasia (BPH) compared to endostatin binding to vessels in normal prostate tissue. Biotinylated endostatin was used and was detected using Extravidin CY3.


RESULTS
In BPH 89.12% +/- 10.72% of vessels showed endostatin binding. This was significantly more than observed for vessels in normal prostate tissue (1.66% +/- 1.66%).


CONCLUSIONS
The strongly proliferative tissue of BPH may be a growth-limited cause of significantly more endostatin binding sites. The investigation indicates endostatin as a possible new target for BPH treatment.
Schmidt
Annette
A
Department of Molecular and Cellular Sport Medicine, German Sport University Cologne, Carl-Diem-Weg 6, 50933 Cologne, Germany. A.Schmidt@dshs-koeln.de
Sommer
Frank
F
Ozgür
Enver
E
Klotz
Theodor
T
Engelmann
Udo
U
Addicks
Klaus
K
Bloch
Wilhelm
W
D000368:Aged; D001665:Binding Sites; D001808:Blood Vessels / Q000378:metabolism; D043169:Endostatins / Q000378:metabolism*; D006801:Humans; D008297:Male; D011467:Prostate / Q000098:blood supply* / Q000378:metabolism*; D011470:Prostatic Hyperplasia / Q000378:metabolism*
D043169:Endostatins