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Glucocorticoids stimulate ENaC upregulation in bovine mammary epithelium.
Am J Physiol Cell Physiol. 2007 May; 292(5):C1739-45.AJ

Abstract

Mammary epithelia produce an isotonic, low-Na(+) fluid that is rich in nutrients. Mechanisms that account for the low electrolyte concentration have not been elucidated, although amiloride-sensitive ion transport has been reported in some situations. We hypothesized that corticosteroid exposure modulates epithelial Na(+) channel (ENaC) expression and/or activity in bovine mammary epithelial cells. BME-UV cells were grown to confluent monolayers on permeable supports with a standard basolateral medium and apical medium of low-electrolyte, high-lactose composition that resembles the ionic composition of milk. Ion transport was assessed in modified Ussing flux chambers. Exposure to glucocorticoids (dexamethasone, cortisol, or prednisolone), but not aldosterone, increased short-circuit current (I(sc)), a sensitive measure of net ion transport, whereas apical exposure to amiloride or benzamil reduced corticosteroid-induced I(sc) close to basal levels. Quantitative RT-PCR indicated a glucocorticoid-induced increase in mRNA for beta- and gamma-ENaC, whereas alpha-ENaC mRNA expression was only mildly affected. Exposure to mifepristone (a glucocorticoid receptor antagonist), but not spironolactone (a mineralocorticoid receptor antagonist), precluded both the corticosteroid-induced elevation in amiloride-sensitive I(sc) and the induced changes in beta- and gamma-ENaC mRNA. We conclude that Na(+) movement across mammary epithelia is modulated by corticosteroids via a glucocorticoid receptor-mediated mechanism that regulates the expression of the beta- and gamma-subunits of ENaC. ENaC expression and activity could account for the low Na(+) concentration that is typical of milk.

Authors+Show Affiliations

Department of Anatomy and Physiology, 228 Coles Hall, Kansas State University, Manhattan, KS 66506, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

17251323

Citation

Quesnell, Rebecca R., et al. "Glucocorticoids Stimulate ENaC Upregulation in Bovine Mammary Epithelium." American Journal of Physiology. Cell Physiology, vol. 292, no. 5, 2007, pp. C1739-45.
Quesnell RR, Han X, Schultz BD. Glucocorticoids stimulate ENaC upregulation in bovine mammary epithelium. Am J Physiol Cell Physiol. 2007;292(5):C1739-45.
Quesnell, R. R., Han, X., & Schultz, B. D. (2007). Glucocorticoids stimulate ENaC upregulation in bovine mammary epithelium. American Journal of Physiology. Cell Physiology, 292(5), C1739-45.
Quesnell RR, Han X, Schultz BD. Glucocorticoids Stimulate ENaC Upregulation in Bovine Mammary Epithelium. Am J Physiol Cell Physiol. 2007;292(5):C1739-45. PubMed PMID: 17251323.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Glucocorticoids stimulate ENaC upregulation in bovine mammary epithelium. AU - Quesnell,Rebecca R, AU - Han,Xiaobin, AU - Schultz,Bruce D, Y1 - 2007/01/24/ PY - 2007/1/26/pubmed PY - 2007/6/22/medline PY - 2007/1/26/entrez SP - C1739 EP - 45 JF - American journal of physiology. Cell physiology JO - Am J Physiol Cell Physiol VL - 292 IS - 5 N2 - Mammary epithelia produce an isotonic, low-Na(+) fluid that is rich in nutrients. Mechanisms that account for the low electrolyte concentration have not been elucidated, although amiloride-sensitive ion transport has been reported in some situations. We hypothesized that corticosteroid exposure modulates epithelial Na(+) channel (ENaC) expression and/or activity in bovine mammary epithelial cells. BME-UV cells were grown to confluent monolayers on permeable supports with a standard basolateral medium and apical medium of low-electrolyte, high-lactose composition that resembles the ionic composition of milk. Ion transport was assessed in modified Ussing flux chambers. Exposure to glucocorticoids (dexamethasone, cortisol, or prednisolone), but not aldosterone, increased short-circuit current (I(sc)), a sensitive measure of net ion transport, whereas apical exposure to amiloride or benzamil reduced corticosteroid-induced I(sc) close to basal levels. Quantitative RT-PCR indicated a glucocorticoid-induced increase in mRNA for beta- and gamma-ENaC, whereas alpha-ENaC mRNA expression was only mildly affected. Exposure to mifepristone (a glucocorticoid receptor antagonist), but not spironolactone (a mineralocorticoid receptor antagonist), precluded both the corticosteroid-induced elevation in amiloride-sensitive I(sc) and the induced changes in beta- and gamma-ENaC mRNA. We conclude that Na(+) movement across mammary epithelia is modulated by corticosteroids via a glucocorticoid receptor-mediated mechanism that regulates the expression of the beta- and gamma-subunits of ENaC. ENaC expression and activity could account for the low Na(+) concentration that is typical of milk. SN - 0363-6143 UR - https://www.unboundmedicine.com/medline/citation/17251323/Glucocorticoids_stimulate_ENaC_upregulation_in_bovine_mammary_epithelium_ L2 - https://journals.physiology.org/doi/10.1152/ajpcell.00369.2006?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -