Cortisol and regulation of tight junctions in the mammary gland of the late-pregnant goat

Thompson, Gregory A.

doi:10.1017/s0022029900031794

Cited by 18 publications

(11 citation statements)

References 11 publications

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“…There is evidence from in vivo studies that glucocorticoids may control the permeability of tight junctions. In late-pregnant goats, an intraluminal injection of cortisol had marked effects on the composition of fluid within the lumen: K ϩ concentration increased and Na ϩ decreased, which is consistent with the closing of tight junctions (224). However, an effect of cortisol on transcellular ion transport cannot be ruled out at this stage.…”

Section: B Solute Transport Via the Paracellular Pathwaymentioning

confidence: 82%

Transport of Milk Constituents by the Mammary Gland

Shennan

Peaker

2000

Physiological Reviews

348

278

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This review deals with the cellular mechanisms that transport milk constituents or the precursors of milk constituents into, out of, and across the mammary secretory cell. The various milk constituents are secreted by different intracellular routes, and these are outlined, including the paracellular pathway between interstitial fluid and milk that is present in some physiological states and in some species throughout lactation. Also considered are the in vivo and in vitro methods used to study mammary transport and secretory mechanisms. The main part of the review addresses the mechanisms responsible for uptake across the basolateral cell membrane and, in some cases, for transport into the Golgi apparatus and for movement across the apical membrane of sodium, potassium, chloride, water, phosphate, calcium, citrate, iodide, choline, carnitine, glucose, amino acids and peptides, and fatty acids. Recent work on the control of these processes, by volume-sensitive mechanisms for example, is emphasized. The review points out where future work is needed to gain an overall view of milk secretion, for example, in marsupials where milk composition changes markedly during development of the young, and particularly on the intracellular coordination of the transport processes that result in the production of milk of relatively constant composition at a particular stage of lactation in both placental and marsupial mammals.

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Section: B Solute Transport Via the Paracellular Pathwaymentioning

confidence: 82%

Transport of Milk Constituents by the Mammary Gland

Shennan

Peaker

2000

Physiological Reviews

348

278

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“…Our study demonstrates that the glucocorticoid down-regulation of RhoA is an integral event in the emergence of this cellular phenotype. Furthermore, our results imply that small GTPases, such as RhoA and Ras, are involved in the in vivo regulation of the tight junctions in the mammary gland, for example during late pregnancy and lactation when glucocorticoid levels are high (81,82). We are currently examining the mechanism by which glucocorticoids down-regulate RhoA protein and are determining the potential in vivo significance of the down-regulation of RhoA and effects on its signaling targets.…”

Section: Effects Of Rhoa On the Glucocorticoid-regulated Organizationmentioning

confidence: 89%

Glucocorticoid Down-regulation of RhoA Is Required for the Steroid-induced Organization of the Junctional Complex and Tight Junction Formation in Rat Mammary Epithelial Tumor Cells

Rubenstein

Guan

Woo

et al. 2003

Journal of Biological Chemistry

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In Con8 mammary epithelial tumor cells, we have documented previously that the synthetic glucocorticoid dexamethasone induces the reorganization of the tight junction and adherens junction (apical junction) and stimulates the monolayer transepithelial electrical resistance (TER), which is a reliable in vitro measurement of tight junction sealing. Western blots demonstrated that dexamethasone treatment down-regulated the level of the RhoA small GTPase prior to the stimulation of the monolayer TER. To test the role of RhoA in the steroid regulation of apical junction dynamics functionally, RhoA levels were altered in Con8 cells by transfection of either constitutively active (RhoA.V14) or dominant negative (RhoA.DN19) forms of RhoA. Ectopic expression of constitutively active RhoA disrupted the dexamethasone-stimulated localization of zonula occludens-1 and ␤-catenin to sites of cell-cell contact, inhibited tight junction sealing, and prevented the complete formation of the F-actin ring structure at the apical side of the cell monolayer. In a complementary manner, dominant negative RhoA caused a precocious organization of the tight junction, adherens junction, and the F-actin rings in the absence of steroid, whereas the monolayer TER remained glucocorticoid-responsive. Taken together, our results demonstrate that the glucocorticoid down-regulation of RhoA is a required step in the steroid signaling pathway which controls the organization of the apical junctional complex and the actin cytoskeleton in mammary epithelial cells.

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“…Further, Thompson (1996) showed that local injection of cortisol into the mammary gland of the late pregnant goat produced a decrease in the sodium, and an increase in the potassium concentration of the mammary secretion product. Using mammary cell cultures on Transwell filters, Firestone and his colleagues (Zettl et al 1992, Woo et al 1999 found that dexamethasone, a powerful glucocorticoid, induced a decrease in tight junction permeability in two different cell types, as measured by transepithelial electrical resistance.…”

Section: Discussionmentioning

confidence: 99%

Hormonal regulation of tight junction closure in the mouse mammary epithelium during the transition from pregnancy to lactation

Da¹,

Af²,

Mc³

2001

Journal of Endocrinology

162

127

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Closure of the tight junctions of the mammary epithelium has been shown to accompany the onset of copious milk secretion or lactogenesis, stage 2, in both goats and humans. Here we use injection of [ 14 C]sucrose and FITC-albumin (fluorescein isothiocyanate-albumin) into the mammary duct to follow the course of tight junction closure during lactogenesis in mice. To examine the hormonal changes responsible, we ovariectomized day 16 or 17 pregnant mice and found that closure followed ovariectomy with a mean delay of 13·6 1·5 (...) h. That progesterone withdrawal is the trigger for closure was shown by the finding that injection of progesterone within 4 h of ovariectomy delayed closure and that closure occurred after injection of the progesterone antagonist RU 486 in intact late pregnant mice. Endocrine ablation studies showed that low to moderate concentrations of corticosterone and either placental lactogen or prolactin are necessary for tight junction closure triggered by progesterone withdrawal. Thus the hormonal requirements for tight junction closure are similar to those shown by other investigators to promote lactogenesis, stage 2. Further, the tight temporal control of tight junction permeability suggests that ovariectomy of the late pregnant mouse may be a good model for molecular studies of the lactogenic switch.

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Cortisol and regulation of tight junctions in the mammary gland of the late-pregnant goat

Cited by 18 publications

References 11 publications

Transport of Milk Constituents by the Mammary Gland

Transport of Milk Constituents by the Mammary Gland

Glucocorticoid Down-regulation of RhoA Is Required for the Steroid-induced Organization of the Junctional Complex and Tight Junction Formation in Rat Mammary Epithelial Tumor Cells

Hormonal regulation of tight junction closure in the mouse mammary epithelium during the transition from pregnancy to lactation

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