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Endocrinology Vol. 139, No. 3 1239-1248
Copyright © 1998 by The Endocrine Society

ARTICLES

Ligand-Dependent Regulation of Retinoic Acid Receptor {alpha} in Rat Testis: In Vivo Response to Depletion and Repletion of Vitamin A

Karin M. Akmal1, Jannette M. Dufour1, Mynuong Vo, Sarah Higginson and Kwan Hee Kim

Department of Genetics and Cell Biology, Department of Biochemistry and Biophysics, Center for Reproductive Biology, Washington State University, Pullman, Washington 99164

Address all correspondence and requests for reprints to: Kwan Hee Kim, Department of Genetics and Cell Biology, Washington State University, Pullman, Washington 99164-4234. E-mail: khkim{at}wsu.edu

Male animals are sterile due to testicular degeneration in the absence of retinoic acid (RA) or functional retinoic acid receptor-{alpha} (RAR{alpha}). This degeneration can be reversed by injecting retinol, a precursor of RA, into vitamin A-deficient (VAD) rats. To determine the relationship between this ligand-dependent testicular degeneration and regeneration and the expression levels of RAR{alpha} messenger RNA and protein, testes were depleted and then replenished with retinol in vivo. Results showed that RAR{alpha} messenger RNA and protein levels declined to VAD amounts after 7 weeks on a VAD diet. This decline was due to decreased RAR{alpha} levels in early meiotic spermatocytes and the loss of advanced germ cells. Interestingly, the advanced germ cells still contained RAR{alpha}, but the protein was primarily cytoplasmic instead of nuclear, indicating inactivity as a transcription factor. In VAD testis, RAR{alpha} levels were low and then increased primarily in Sertoli cells after retinol replenishment. TUNEL analyses showed that most germ cells at the basal aspect of seminiferous tubules were undergoing apoptosis during degeneration. These results indicate that RAR{alpha} is either down-regulated or inactivated in RA-deficient testis and coincident with that, testes degenerate by apoptosis or selective loss of germ cells.




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