Oestradiol decreases colonic permeability through oestrogen receptor β‐mediated up‐regulation of occludin and junctional adhesion molecule‐A in epithelial cells

Braniste, Viorica; Lévêque, Mathilde; Buisson-Brenac, Claire; Buéno, Lionel; Fioramonti, Jean; Houdeau, Eric

doi:10.1113/jphysiol.2009.169300

Cited by 131 publications

(120 citation statements)

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“…Estrogen significantly inhibits occludin expression at the mRNA and protein level after 24 h. This was consistent with previous reports showing that estrogens are able to regulate occludin expression through ER beta in intestinal epithelial cells [42,43]. Sade et al were the first to describe the occludin promoter and suggested tissue type-dependent expression.…”

Section: Discussionsupporting

confidence: 90%

“…To show that MCF-7 cells have these features, we evaluated the effects of E2 on the expression of CRB3, a novel epithelial marker [15], and N-cadherin, a mesenchymal marker. CRB3 is the human ortholog of the crumbs (CRB) protein and is required to establish the apical membrane, define the basolateral plasma domain, and has a fundamental function in the establishment of morphogenesis of 3D epithelial cell cultures [43]. CRB3 is a tumor suppressor during the transformation and progression of mammalian epithelial cells; its loss favors tumor cell growth, metastasis, and EMT [15,44].…”

Section: Discussionmentioning

confidence: 99%

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Membrane-Initiated Estradiol Signaling of Epithelial-Mesenchymal Transition-Associated Mechanisms Through Regulation of Tight Junctions in Human Breast Cancer Cells

et al. 2014

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Tumor cells utilize inappropriate epithelialmesenchymal transition (EMT) mechanisms during the invasive process. It is becoming increasingly clear that estradiol (E2) induces breast cancer cell progression and enhances EMT; however, the mechanisms associated with this are unclear. We investigated the role of E2 on the expression and intracellular localization of the tight junction (TJ)-associated proteins, zonula occluden 1 (ZO-1), ZO-1-associated nucleic acid binding (ZONAB), and occludin, on the activation of cSrc and human epidermal growth factor receptor 2 (HER2) expression and cellular migration in the estrogen receptor (ER)-positive breast cancer cell lines, MCF-7 and T47D. WeNovelty and Impact Statements We demonstrated that estrogen is able to induce tight junction (TJ) disruption in two breast cancer cell lines through the activation of c-Src. Ablated expression of the novel epithelial marker CRB3 could lead to increased cell migration. Based on our findings, we propose a novel estrogen-induced TJ pathway associated with breast cancer cell motility and, eventually, to metastasis. demonstrated that 1 nM E2 elicits c-Src activation after 15 min. The p-Src/ZO-1 complex led to ZO-1 and ZONAB disruption at the TJ and increased expression of HER2 mRNAs. These changes correlate with decreased expression of the epithelial markers occludin and CRB3 and increased synthesis of N-cadherin. This led to increased MCF-7 cell migration induced by E2, even in the presence of a cell proliferation inhibitor. Incubation with ICI 182,780 (Fulvestrant), an ER antagonist, precluded the effects of E2 on c-Src phosphorylation, p-Src/ZO-1 complex formation, ZO-1/ZONAB nuclear translocation, and migration of MCF-7 cells. Our findings suggest that E2 promotes TJ disruption during tumor progression and increases cell motility. We propose a novel pathway where estrogens promote EMTassociated mechanisms that possibly lead to metastasis.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Membrane-Initiated Estradiol Signaling of Epithelial-Mesenchymal Transition-Associated Mechanisms Through Regulation of Tight Junctions in Human Breast Cancer Cells

et al. 2014

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“…This intriguing difference illustrates the importance of considering cell line data in conjunction with more pathophysiologically-representative tissue data from a large number of patients. However since stimulation of ER-β with estrogen has been shown to upregulate JAM-A in intestinal cells (Braniste et al, 2009), we speculate that a level of unexplored crosstalk exists. Given the functionally opposing roles of ER-α and -β in breast tissue, it is possible that ER-α negative tissue may express ER-β, however a larger ER-negative cohort of tissue samples would be needed to answer this question.…”

Section: Resultsmentioning

confidence: 91%

Junctional adhesion molecule-A is co-expressed with HER2 in breast tumors and acts as a novel regulator of HER2 protein degradation and signaling

et al. 2012

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“…Estradiol affects colonic paracellular permeability (CPP) through ERs in epithelial cells (27). OVX rats were used for complete depletion of endogenous sex hormones, and the influence of a daily oral exposure to BPA was examined on CPP in Ussing chambers.…”

Section: Resultsmentioning

confidence: 99%

“…Altogether, a sex difference in intestinal permeability and inflammation (22), the prevalence of irritable bowel syndrome in women (23), the fluctuations of irritable bowel syndrome-associated abdominal pain in women during their menstrual cycle (24), as well as the wide expression of estrogen receptors (ERs) in human fetal and adult colonic mucosa (25,26) suggest that estrogens play a key role. In animal studies, estrogen action on intestinal permeability, inflammation, and viscerosensitivity are controlled by ERs in gut epithelial cells and sensory neurons, the latter conveying peripheral information to the central nervous system (27)(28)(29). Therefore, we assumed that BPA may target these receptors.…”

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confidence: 99%

Impact of oral bisphenol A at reference doses on intestinal barrier function and sex differences after perinatal exposure in rats

Braniste¹,

Jouault²,

Gaultier³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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Bisphenol A (BPA), a chemical estrogen widely used in the foodpackaging industry and baby bottles, is recovered in human fluids (0.1-10 nM). Recent studies have reported that BPA is hormonally active at low doses, emphasizing the debate of a risk for human health. Estrogen receptors are expressed in the colon, and although the major route of BPA exposure is food, the effects on gut have received no attention. We first examined the endocrine disrupting potency of BPA on colonic paracellular permeability (CPP), experimental colitis, and visceral sensitivity in ovariectomized rats orally exposed to 5 mg/kg/d BPA (i.e., the no observed adverse effect level), 50 μg/kg/d BPA (i.e., tolerable daily intake), or lower doses. BPA dosedependently decreased basal CPP, with a half-maximal inhibitory dose of 5.2 μg/kg/d, 10-fold below the tolerable daily intake. This correlated with an increase in epithelial tight junction sealing, also observed in Caco-2 cells exposed to 10 nM BPA. When ovariectomized rats were fed with BPA at the no observed adverse effect level, the severity of colitis was reduced, whereas the same dose increased pain sensitivity to colorectal stimuli. We then examined the impact of perinatal exposure to BPA on intestinal permeability and inflammatory response in the offspring. In female rats, but not in male rats, perinatal BPA evoked a decrease of CPP in adulthood, whereas the proinflammatory response of colonic mucosa was strengthened. This study first demonstrates that the xenoestrogen BPA at reference doses influences intestinal barrier function and gut nociception. Moreover, perinatal exposure promotes the development of severe inflammation in adult female offspring only.endocrine disruptor | gut permeability | inflammation | pain | estrogen

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Oestradiol decreases colonic permeability through oestrogen receptor β‐mediated up‐regulation of occludin and junctional adhesion molecule‐A in epithelial cells

Cited by 131 publications

References 51 publications

Membrane-Initiated Estradiol Signaling of Epithelial-Mesenchymal Transition-Associated Mechanisms Through Regulation of Tight Junctions in Human Breast Cancer Cells

Membrane-Initiated Estradiol Signaling of Epithelial-Mesenchymal Transition-Associated Mechanisms Through Regulation of Tight Junctions in Human Breast Cancer Cells

Junctional adhesion molecule-A is co-expressed with HER2 in breast tumors and acts as a novel regulator of HER2 protein degradation and signaling

Impact of oral bisphenol A at reference doses on intestinal barrier function and sex differences after perinatal exposure in rats

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