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Division of Basic Science Research Department of Obstetrics and Gynecology University of Louisville Health Sciences Center Louisville, Kentucky 40292
LH/hCG receptors were disrupted by gene
targeting in embryonic stem cells. The disruption resulted in
infertility in both sexes. The gonads contained no receptor mRNA or
receptor protein. Serum LH levels were greatly elevated, and FSH levels
were moderately elevated in both sexes; estradiol and progesterone
levels decreased but were not totally suppressed in females;
testosterone levels were dramatically decreased and estradiol levels
moderately elevated in males. The external and internal genitalia were
grossly underdeveloped in both sexes. Abnormalities included
ambiguous vaginal opening, abdominal testes, micropenis,
dramatically decreased weights of the gonads and reproductive tract,
arrested follicular growth beyond antral stage, disarray of
seminiferous tubules, diminished number and hypotrophy of Leydig
cells, and spermatogenic arrest beyond the round spermatid stage.
LH/hCG receptor gene disruption had no effect on FSH receptor mRNA
levels in ovaries and testes, progesterone receptor (PR) levels in
ovaries and androgen receptor (AR) levels in testes. However, it caused
a dramatic decrease in StAR and estrogen receptor-
(ER) mRNA
levels and an increase in ERß mRNA levels in both ovaries and testes.
Estradiol and progesterone replacement therapy in females and
testosterone replacement in males, to determine whether
phenotype and biochemical changes were a consequence of decreased
gonadal steroid levels or due to a loss of LH signaling, revealed
complete restoration of some and partial restoration of others.
Nevertheless, the animals remained infertile. It is anticipated that
the LH receptor knockout animals will increase our current
understanding of gonadal and nongonadal actions of LH and hCG.
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