Female Reproductive Tract

Impairment of Decidualization in SRC-Deficient Mice

Abstract
Many signaling events induced by ovarian steroid hormones, cytokines, and growth factors are involved in the process of decidualization of human and rodent endometrium. We have previously reported that tyrosine kinase activation of SRC functionally participates in decidualization of human endometrial stromal cells. To address its essential role in decidualization, we here examined using wild-type and Src knockout mice whether decidualization process was impaired in the absence of SRC. Immunohistochemistry using an antibody specific for the active form of SRC revealed that the active SRC was prominently expressed in the decidualizing stromal cells of the pregnant wild-type mouse. Moreover, the active SRC was up-regulated in the uterine horn with artificially stimulated decidual reaction. In comparison with wild-type and Src heterozygous mice, the uterus of Src null mice showed no apparent decidual response following artificial stimulation. Ovarian steroid-induced decidualization in vitro, as determined by morphological changes and expression of decidual/trophoblast prolactin-related protein and prostaglandin-endoperoxide synthase 2 (also known as Cox2), both decidualization markers, did not timely occur in endometrial stromal cells isolated from the uteri of SRC-deficient mice as compared to those of wild-type and Src heterozygous mice. Our results collectively suggest that SRC is an indispensable signaling component for maximal decidualization in mice.

Key words: Female Reproductive Tract • Decidua • Estradiol • Kinases • Progesterone

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