Modulation of gap junction transcript and protein expression during pregnancy in the rat.

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Abstract
The expression of three different gap junction transcripts, .alpha.1 (Cx43), .beta.1 (Cx32), and .beta.2 (Cx26) was examined in several organs during pregnancy in the rat. In all of the organs that were examined - uterus, ovary, heart, and liver - there was a strong correlation between levels of gap junction mRNA and gap junction antigens that were detected at different stages of pregnancy. A striking change in .alpha.1 transcript levels (a 5.5-fold increase) was detected in the uterine myometrium on the day before parturition. This elevation of the .alpha.1 transcript is thought to be associated with the formation of gap junctions that are required for synchronizing the contractility of the myometrial cells during parturition. 2 d before parturition, there was a detectable elevation of .beta.2 transcripts and protein in the endometrial epithelium, which was then followed by a dramatic decrease in .beta.2 gap junctional protein on the day before parturition. There was also a substantial elevation of .alpha.1 transcripts (a 6.7-fold increase) in the stromal regions of the ovary on the day before parturition that was identical to the temporal pattern of .alpha.1 expression in the myometrium. In all three instances - the .alpha.1 transcripts in the myometrium, .beta.2 transcripts in the endometrium, and .alpha.1 transcripts in the ovary - the transcript modulation appeared to be cell specific, because the changes in transcript levels of these three gene products occurred independently of the poly(A) + RNA concentrations at the same pregnancy stages in the respective organs. There were no specific changes detected in gap junction transcript levels in the heart and liver during pregnancy. These observations indicate that a cell-specific modulation of gap junction expression occurs in two regions of the uterus and the ovary during pregnancy. Further, it appears that the same gap junction gene in different organs, such as the .alpha.1 gene in the uterine myometrium and the heart, can be differentially regulated.