{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T20:06:06Z","timestamp":1785182766702,"version":"3.55.0"},"reference-count":36,"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":[[2012,9,15]]},"abstract":"<jats:p> Opiates have been reported to induce T cell loss. We evaluated the role of vitamin D receptor (VDR) and the activation of the renin-angiotensin system (RAS) in morphine-induced T cell loss. Morphine-treated human T cells displayed downregulation of VDR and the activation of the RAS. On the other hand, a VDR agonist (EB1089) enhanced T cell VDR expression both under basal and morphine-stimulated states. Since T cells with silenced VDR displayed the activation of the RAS, whereas activation of the VDR was associated with downregulation of the RAS, it appears that morphine-induced T cell RAS activation was dependent on the VDR status. Morphine enhanced reactive oxygen species (ROS) generation in a dose-dependent manner. Naltrexone (an opiate receptor antagonist) inhibited morphine-induced ROS generation and thus, suggested the role of opiate receptors in T cell ROS generation. The activation of VDR as well as blockade of ANG II (by losartan, an AT<jats:sub>1<\/jats:sub> receptor blocker) also inhibited morphine-induced T cell ROS generation. Morphine not only induced double-strand breaks (DSBs) in T cells but also attenuated DNA repair response, whereas activation of VDR not only inhibited morphine-induced DSBs but also enhanced DNA repair. Morphine promoted T cell apoptosis; however, this effect of morphine was inhibited by blockade of opiate receptors, activation of the VDR, and blockade of the RAS. These findings indicate that morphine-induced T cell apoptosis is mediated through ROS generation in response to morphine-induced downregulation of VDR and associated activation of the RAS. <\/jats:p>","DOI":"10.1152\/ajpcell.00076.2012","type":"journal-article","created":{"date-parts":[[2012,7,4]],"date-time":"2012-07-04T22:37:59Z","timestamp":1341441479000},"page":"C607-C615","source":"Crossref","is-referenced-by-count":11,"title":["Vitamin D receptor activation and downregulation of renin-angiotensin system attenuate morphine-induced T cell apoptosis"],"prefix":"10.1152","volume":"303","author":[{"given":"Nirupama","family":"Chandel","sequence":"first","affiliation":[{"name":"Immunology Center, Feinstein Institute for Medical Research, Hofstra North Shore LIJ Medical School, Great Neck, New York; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bipin","family":"Sharma","sequence":"additional","affiliation":[{"name":"Immunology Center, Feinstein Institute for Medical Research, Hofstra North Shore LIJ Medical School, Great Neck, New York; 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