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Motoyuki Otsuka, Min Zheng, Masaaki Hayashi, Jing-Dwan Lee, Osamu Yoshino, Shengcai Lin, Jiahuai Han
Published in Volume 118, Issue 5
J Clin Invest. 2008; 118(5):1944–1954 doi:10.1172/JCI33680
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Figure 1
CL insufficiency is the cause of Dicerd/d female mouse infertility.

(A) Fertility of Dicerd/d female mice transplanted with Dicer+/+ ovaries. Ovaries of Dicerd/d and Dicer+/+ littermate mice were exchanged (n = 8 pairs), and the mice were subsequently bred to wild-type fertile males. Delivery rate and average litter size are shown. (B and C) Ovulation and fertilization were normal in Dicerd/d mice. (B) Representative morphologies of the 2 cell embryos collected from the oviducts of Dicerd/d mice on day 1.5 after coitus. Original magnification, ×100 (top), ×400 (bottom). (C) Rates of ovulation and fertilization in Dicerd/d and Dicer+/+ mice were examined on day 1.5 with or without superovulation. (D) Serum progesterone levels were lower in Dicerd/d mice during pregnancy. Serum levels of progesterone in Dicerd/d mice were determined by ELISA on days 1.5, 5.5, and 7.5 of pregnancy and expressed as mean ± SD (n = 3). (E) The expression of genes associated with CL function was lower in Dicerd/d mice. Semiquantitative RT-PCR analyses of luteinizing hormone receptor, prolactin receptor, and cytochrome P450 family 11 subfamily a polypeptide 1 mRNA in ovaries of Dicerd/d and Dicer+/+ mice were conducted on days 1.5, 5.5, and 7.5 after coitus. Results from 2 separate littermate samples are shown.