{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T01:27:04Z","timestamp":1791163624443,"version":"4.1.0"},"reference-count":29,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Cell Physiology"],"published-print":{"date-parts":[[1997,12,1]]},"abstract":"<jats:p> Interferon-\u03b3 (IFN-\u03b3) \u00b1 tumor necrosis factor-\u03b1 (TNF-\u03b1) induces antiproliferation and intracellular Ca<jats:sup>2+<\/jats:sup> store depletion in a human submandibular ductal cell line (HSG), which can be reversed on cytokine removal [A. J. Wu, G. C. Chen, B. J. Baum, and I. S. Ambudkar. Am. J. Physiol. 270 ( Cell Physiol. 39): C514\u2013C521, 1996]. Here we have examined a possible mechanism for the IFN-\u03b3-induced intracellular Ca<jats:sup>2+<\/jats:sup>store depletion. There was a time-dependent decrease in thapsigargin-dependent internal Ca<jats:sup>2+<\/jats:sup> release after exposure of the cells to the cytokines. The intracellular Ca<jats:sup>2+<\/jats:sup> pump [sarco(endo)plasmic reticulum Ca<jats:sup>2+<\/jats:sup>-ATPase (SERCA)] protein in lysates and membranes of cells treated with IFN-\u03b3 \u00b1 TNF-\u03b1, but not with TNF-\u03b1 alone, showed a similar time-dependent decrease (examined using a SERCA2 antibody). Removal of the cytokines, which resulted in recovery of cell growth and refill of internal Ca<jats:sup>2+<\/jats:sup> stores, also increased the level of SERCA protein. The decrease in SERCA is not a result of decreased cell proliferation, since thapsigargin, 2,5-di-( t-butyl)-1,4-hydroquinone, or serum-free growth conditions induced antiproliferative effects on HSG cells without any corresponding decrease in SERCA. We suggest that the IFN-\u03b3-induced decrease in the level of SERCA accounts for the depleted state of internal Ca<jats:sup>2+<\/jats:sup>stores in cytokine-treated HSG cells. These data suggest a novel mechanism for the inhibition of HSG cell growth by IFN-\u03b3. <\/jats:p>","DOI":"10.1152\/ajpcell.1997.273.6.c2030","type":"journal-article","created":{"date-parts":[[2017,12,24]],"date-time":"2017-12-24T17:00:16Z","timestamp":1514134816000},"page":"C2030-C2036","source":"Crossref","is-referenced-by-count":23,"title":["Interferon-\u03b3 induces a decrease in the intracellular  calcium pump in a human salivary gland cell line"],"prefix":"10.1152","volume":"273","author":[{"given":"Sean","family":"Meehan","sequence":"first","affiliation":[{"name":"Secretory Physiology Section, Gene Therapy and Therapeutics Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ava J.","family":"Wu","sequence":"additional","affiliation":[{"name":"Secretory Physiology Section, Gene Therapy and Therapeutics Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elaine C.","family":"Kang","sequence":"additional","affiliation":[{"name":"Secretory Physiology Section, Gene Therapy and Therapeutics Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takayuki","family":"Sakai","sequence":"additional","affiliation":[{"name":"Secretory Physiology Section, Gene Therapy and Therapeutics Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Indu S.","family":"Ambudkar","sequence":"additional","affiliation":[{"name":"Secretory Physiology Section, Gene Therapy and Therapeutics Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1177\/10454411930040032301"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.9.15.8529837"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/nm0695-534"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.267.5.C1398"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.52.030190.003045"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.267.2.C402"},{"key":"B7","doi-asserted-by":"crossref","first-page":"5532","DOI":"10.4049\/jimmunol.152.11.5532","volume":"152","author":"Fox R. 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