Cellular localization and steroid hormone regulation of mRNA encoding tumour necrosis factor receptor I in mouse uterus

Abstract

Signals transduced by binding of tumour necrosis factor alpha (TNF) and lymphotoxin alpha (LT-alpha) trimers to high-affinity cell membrane receptors, TNF-RI (p55/p60) and TNF-RII (p75/p80), affect many cell functions. In this study, expression of the gene encoding TNF-RI in uteri of cyclic mice was mapped using in situ hybridization. TNF-RI hybridization signals fluctuated during the cycle. Signal intensity was highest during dioestrus-II, when mRNA encoding TNF-RI was present in endometrial epithelial and stroma cells, as well as in myometrial smooth muscle and connective tissue cells. The ability of oestradiol and progesterone to modulate steady state concentrations of mRNA encoding TNF-RI in uterine cells was assessed by using in situ and northern blot hybridization procedures. Seven days after ovariectomy, low concentrations of mRNA encoding TNF-RI were detected by northern analysis and weak in situ hybridization signals were identified in epithelia and some myometrial connective tissue cells. Administration of oestradiol, progesterone or oestradiol plus progesterone to ovariectomized animals stimulated temporal and cell type-specific changes in steady state concentrations of mRNA encoding TNF-RI that were unique to each hormonal regimen. Maximal induction of mRNA encoding TNF-RI required 24 h of oestradiol stimulation and 72 h of progesterone stimulation. In uteri treated with oestradiol plus progesterone, the oestradiol pattern predominated over the progesterone pattern. Thus, multiple cell types in cyclic mouse uteri express the gene encoding TNF-RI, and expression in specific cells is controlled by female steroid hormones.