Lim H, Paria B C, Das S K, Dinchuk J E, Langenbach R, Trzaskos J M, Dey S K
Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City 66160, USA.
Cell. 1997 Oct 17;91(2):197-208. doi: 10.1016/s0092-8674(00)80402-x.
Cyclooxygenase (COX) is the rate-limiting enzyme in the synthesis of prostaglandins (PGs) and exists in two isoforms, COX-1 and COX-2. In spite of long-standing speculation, definitive roles of PGs in various events of early pregnancy remain elusive. We demonstrate herein that the targeted disruption of COX-2, but not COX-1, in mice produces multiple failures in female reproductive processes that include ovulation, fertilization, implantation, and decidualization. Using multiple approaches, we conclude that these defects are the direct result of target organ-specific COX-2 deficiency but are not the result of deficiency of pituitary gonadotropins or ovarian steroid hormones, or reduced responsiveness of the target organs to their respective hormones.
环氧化酶（COX）是前列腺素（PGs）合成中的限速酶，以两种同工型COX-1和COX-2存在。尽管长期以来一直有推测，但PGs在早期妊娠各种事件中的明确作用仍不清楚。我们在此证明，在小鼠中靶向破坏COX-2而非COX-1会导致雌性生殖过程出现多种缺陷，包括排卵、受精、着床和蜕膜化。通过多种方法，我们得出结论，这些缺陷是靶器官特异性COX-2缺乏的直接结果，而非垂体促性腺激素或卵巢甾体激素缺乏，也不是靶器官对各自激素反应性降低的结果。
