Identification and localization of estrogen receptor a- and �-positive cells in adult male and female mouse intestine at various estrogen levels

Abstract

Although estrogen is implicated in the regulation of mammalian intestinal function, the presence and the distribution of estrogen receptor (ER)-positive cells in the intestine are still controversial. The present study was designed to localize ERalpha- and ERbeta-expressing cells in female and male mouse intestines immunohistochemically under various estrogen conditions, especially in female mice, ovariectomized as well at various phases of the estrous cycle. Western blot analysis detected both ERalpha (66-kDa band) and ERbeta (56-kDa band). Immunohistochemical staining of paraffin-embedded sections after antigen-retrieval treatment with autoclaving revealed staining for ERalpha in submucosal interstitial cells, and double staining identified these cells as a subtype of intestinal macrophages. The number of these cells varied according to the estrous cycle phase. Administration of 17beta-estradiol to ovariectomized mice resulted in a significant increase in the number of ERalpha-positive macrophages. On the other hand, the nuclei of nerve cells in Auerbach and Meissner plexuses were positive for both ERalpha and ERbeta, but the number of positive nerve cells was not affected by estrogen. Our results indicate that estrogen and estrogenic compounds may exert their actions on the intestine in two ways; one is through interstitial macrophages and the other is through intestinal neurons.

Host Responses to the Pathogen Mycobacterium avium subsp. paratuberculosis and Beneficial Microbes Exhibit Host Sex Specificity

“…Women are 30% more likely to develop irritable bowel disease than men (57,58). Studies have demonstrated estrogen to be contributive to GIT diseases, but the specific mechanisms associated with its action are largely understudied (57)(58)(59)(60)(61). Both females and males produce estrogen and estrogen receptors in GIT tissues, and learning more about these biological relationships could elucidate unexplored niches in disease (61)(62)(63)(64).…”

“…Studies have demonstrated estrogen to be contributive to GIT diseases, but the specific mechanisms associated with its action are largely understudied (57)(58)(59)(60)(61). Both females and males produce estrogen and estrogen receptors in GIT tissues, and learning more about these biological relationships could elucidate unexplored niches in disease (61)(62)(63)(64). Equally, exploring testosterone and its properties could also lead to new understanding of the connections between the endocrine, immune, GIT, and nervous systems (61)(62)(63)(64).…”

Circulating hormones and estrous stage predict cellular and stromal remodeling in murine uterus

“…In complete contrast, another study (Carley et al 2003) reported that uterine ERa expression significantly increased following ovariectomy when compared with sham-operated mice, while ERb levels remained unchanged. In a study of mouse intestinal macrophages, the number of ERa-positive macrophages varied with the stage of estrous, and ovariectomy resulted in fewer ERa-positive macrophages (Kawano et al 2004). Thus, ovariectomy itself can lead to a change in the expression of ERa and the subsequent response to exogenous hormone treatment, obscuring significant cyclical effects of the estrous cycle.…”

Estrogen-dependent regulation of sodium/hydrogen exchanger-3 (NHE3) expression via estrogen receptor β in proximal colon of pregnant mice

“…ERs are products of diVerent genes and exhibit tissue-and cell-type speciWc expression (Sar and Welsch 1999;Matthews and Gustafsson 2003). The presence of ER has been reported in rodent colon (Kawano et al 2004;Wada-Hiraike et al 2006), human colon cancer (Castiglione et al 2008;Giroux et al 2008), and cancer cell line (Campbell-Thompson et al 2001, Martineti et al 2005) and determined as a predominant ER subtype in the colon. However, the functional role of ER in the colon is not fully understood.…”

“…Estrogen plays a critical role in maintaining the structure and function of various reproductive (Pelletier and El-Alfy 2000;Wang et al 2000;Ulziibat et al 2006) and nonreproductive organs (Nishihara et al 2000;Tsurusaki et al 2003;Kawano et al 2004;Shukuwa et al 2006). In general, the biological actions of estrogen are mediated through its binding to its receptors, estrogen receptor (ER)-, and ER , which then bind to the estrogen response element (ERE), which is harbored in the promoter region of various estrogen-dependent genes (Klinge 2001;Marzouk et al 2008).…”