{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,15]],"date-time":"2026-08-15T10:48:59Z","timestamp":1786790939808,"version":"build-2736575974"},"reference-count":50,"publisher":"Frontiers Media SA","issue":"5","license":[{"start":{"date-parts":[[2009,5,1]],"date-time":"2009-05-01T00:00:00Z","timestamp":1241136000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Exp Biol Med (Maywood)"],"published-print":{"date-parts":[[2009,5]]},"abstract":"<jats:p>\n                    Glucocorticoids and mineralocorticoids modulate Na\n                    <jats:sup>+<\/jats:sup>\n                    transport via epithelial Na\n                    <jats:sup>+<\/jats:sup>\n                    channels (ENaC). The rat submandibular epithelial cell line, SMG-C6, expresses \u03b1-ENaC mRNA and protein and exhibits amiloride-sensitive Na\n                    <jats:sup>+<\/jats:sup>\n                    transport when grown in low-serum (2.5%) defined medium, therefore, we examined the effects of altering the composition of the SMG-C6 cell growth medium on ENaC expression and function. No differences in basal or amiloride-sensitive short-circuit current (I\n                    <jats:sub>sc<\/jats:sub>\n                    ) were measured across SMG-C6 monolayers grown in the absence of thyroid hormone, insulin, transferrin, or EGF. In the absence of hydrocortisone, basal and amiloride-sensitive I\n                    <jats:sub>sc<\/jats:sub>\n                    significantly decreased. Similarly, monolayers grown in 10% serum-supplemented medium had lower basal I\n                    <jats:sub>sc<\/jats:sub>\n                    and no response to amiloride. Adding hydrocortisone (1.1 \u03bcM) to either the low or 10% serum medium increased basal and amiloride-sensitive I\n                    <jats:sub>sc<\/jats:sub>\n                    , which was blocked by RU486, the glucocorticoid and progesterone receptor antagonist. Aldosterone also induced an increase in \u03b1-ENaC expression and Na\n                    <jats:sup>+<\/jats:sup>\n                    transport, which was also blocked by RU486 but not by the mineralocorticoid receptor antagonist spironolactone. Thus, in the SMG-C6 cell line, hydrocortisone and aldosterone increased ENaC expression and basal epithelial Na\n                    <jats:sup>+<\/jats:sup>\n                    transport. The absence of endogenous ENaC expression in culture conditions devoid of steroids makes the properties of this cell line an excellent model for investigating pathways regulating ENaC expression and Na\n                    <jats:sup>+<\/jats:sup>\n                    transport.\n                  <\/jats:p>","DOI":"10.3181\/0806-rm-209","type":"journal-article","created":{"date-parts":[[2009,2,21]],"date-time":"2009-02-21T22:51:55Z","timestamp":1235256715000},"page":"522-531","source":"Crossref","is-referenced-by-count":15,"title":["Regulation of Epithelial Na\n                    <sup>+<\/sup>\n                    Channel (ENaC) in the Salivary                Cell Line SMG-C6"],"prefix":"10.3389","volume":"234","author":[{"given":"Margarita M.","family":"Vasquez","sequence":"first","affiliation":[{"name":"Department of Pediatrics\/Division of\r               Neonatology, University of Texas Health Science Center at San Antonio, San Antonio,\r               Texas 78229-3900"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shamimunisa B.","family":"Mustafa","sequence":"additional","affiliation":[{"name":"Department of Pediatrics\/Division of\r               Neonatology, University of Texas Health Science Center at San Antonio, San Antonio,\r               Texas 78229-3900"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ahsan","family":"Choudary","sequence":"additional","affiliation":[{"name":"Department of Pediatrics\/Division of\r               Neonatology, University of Texas Health Science Center at San Antonio, San Antonio,\r               Texas 78229-3900"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steve R.","family":"Seidner","sequence":"additional","affiliation":[{"name":"Department of Pediatrics\/Division of\r               Neonatology, University of Texas Health Science Center at San Antonio, San Antonio,\r               Texas 78229-3900"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert","family":"Castro","sequence":"additional","affiliation":[{"name":"Department of Pediatrics\/Division of\r               Neonatology, University of Texas Health Science Center at San Antonio, San Antonio,\r               Texas 78229-3900"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2009,5,1]]},"reference":[{"key":"bibr-R1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.61.1.627"},{"key":"bibr-R2","doi-asserted-by":"publisher","DOI":"10.1385\/CBB:36:2-3:105"},{"key":"bibr-R3","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1997.77.2.359"},{"key":"bibr-R4","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(96)80023-8"},{"key":"bibr-R5","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.62.1.573"},{"key":"bibr-R6","doi-asserted-by":"publisher","DOI":"10.1038\/367463a0"},{"key":"bibr-R7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI7869"},{"key":"bibr-R8","doi-asserted-by":"crossref","unstructured":"Barker PM, Gatzy JT. 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