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Growth Factor-Stimulated Mitogen-Activated Kinase (MAPK) Phosphorylation in the Rat Epididymis Is Limited by Segmental Boundaries¹

Departments of Urology³ Cell Biology,⁴ University of Virginia, School of Medicine, Charlottesville, Virginia 22908

ABSTRACT

Previous evidence has shown that sperm maturation is the result of successive events that influence sperm cells as they move through different microenvironments from the caput to the cauda epididymis. The physiological basis for the creation and maintenance of specific microenvironments along the epididymis are poorly understood. Anatomically, the epididymis consists of segments or lobules of epididymal tubule separated by connective tissue septa (CTS). The fact that CTS restrict the diffusion of tracer substances between segments and that certain gene expression patterns are segment-specific suggest that segments may represent functional epididymal units. In this report, we have further investigated epididymal segmentation by focusing on the ability of CTS to limit the effect of biologically relevant molecules, in particular epidermal growth factor (EGF), basic fibroblast growth factor (FGF2), and vascular endothelial growth factor A (VEGFA), in Segments 1 and 2 of the rat epididymis. We have demonstrated that these growth factors activate mitogen-activated kinase (MAPK) in both segments studied and that growth factors injected into the interstitial space of these segments in vivo exhibited a stimulatory effect only in the segment into which they were injected, i.e., MAPK activation was not observed in the adjacent segment. This restricting influence of CTS was abrogated by treatment with collagenase. In addition, we demonstrate the expression of selected forms of these growth factors and their receptors in Segments 1 and 2, and identify potential downstream targets. These results suggest that CTS regulate the trophic influences of growth factors and potentially other paracrine molecules, thus creating functionally separate units within the epididymis.

epididymis, growth factors, kinases, male reproductive tract, signal transduction

¹ Supported by NIH grants P50-DK45179 and T32-HDO7382.

² Correspondence: Terry T. Turner, Department of Urology, University of Virginia School of Medicine, P.O. Box 800422, Charlottesville, VA 22908. FAX: 434-924-8311; ttt{at}virginia.edu