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J. Cell Biol.,
Volume 143, Number 6, December 14, 1998 1705-1712
* Molecular/Cancer Biology Laboratory, Haartman Institute and Vascular endothelial growth factor (VEGF)
is a key regulator of endothelial growth and permeability. However, VEGF may also target nonendothelial
cells, as VEGF receptors and responsiveness have been
detected for example in monocytes, and high concentrations of VEGF have been reported in human semen.
In this work we present evidence that overexpression of
VEGF in the testis and epididymis of transgenic mice
under the mouse mammary tumor virus (MMTV) LTR
promoter causes infertility. The testes of the transgenic mice exhibited spermatogenic arrest and increased capillary density. The ductus epididymidis was dilated,
containing areas of epithelial hyperplasia. The number
of subepithelial capillaries in the epididymis was also
increased and these vessels were highly permeable as judged by the detection of extravasated fibrinogen
products. Intriguingly, the expression of VEGF receptor-1 (VEGFR-1) was detected in certain spermatogenic cells in addition to vascular endothelium, and
both VEGFR-1 and VEGFR-2 were also found in the
Leydig cells of the testis. The infertility of the MMTV-VEGF male mice could thus result from VEGF acting
on both endothelial and nonendothelial cells of the
male genital tract. Taken together, these findings suggest that the VEGF transgene has nonendothelial target cells in the testis and that VEGF may regulate male
fertility.
Biotechnology Institute, University of Helsinki, 00014 Helsinki, Finland; and § Institute of Biomedicine, Department of Anatomy, University of Turku, 20520 Turku, Finland
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