{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,4]],"date-time":"2026-11-04T23:22:56Z","timestamp":1793834576104,"version":"4.6.1"},"reference-count":30,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)","doi-asserted-by":"publisher","award":["HL126301"],"award-info":[{"award-number":["HL126301"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)","doi-asserted-by":"publisher","award":["HL105324"],"award-info":[{"award-number":["HL105324"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)","doi-asserted-by":"publisher","award":["HD067541"],"award-info":[{"award-number":["HD067541"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000968","name":"American Heart Association (AHA)","doi-asserted-by":"publisher","award":["16SDG27520000"],"award-info":[{"award-number":["16SDG27520000"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Regulatory, Integrative and Comparative Physiology"],"published-print":{"date-parts":[[2016,12,1]]},"abstract":"<jats:p> Preeclampsia is associated with chronic inflammation and an imbalance among T-helper cell subtypes with an increase in T-helper 17 (T<jats:sub>H<\/jats:sub>17) cells. The objective of this study was to determine a role for T<jats:sub>H<\/jats:sub>17s, from the reduced uterine perfusion pressure (RUPP) rat model of preeclampsia, in the etiology of hypertension and chronic inflammation during pregnancy. CD4<jats:sup>+<\/jats:sup>\/CD25<jats:sup>\u2212<\/jats:sup> T cells were isolated from rat spleens, cultured in T<jats:sub>H<\/jats:sub>17 media, and were verified as T<jats:sub>H<\/jats:sub>17s via flow cytometry. On day 12 of gestation, 1\u00d710<jats:sup>6<\/jats:sup> T<jats:sub>H<\/jats:sub>17 cells from RUPP rats were adoptively transferred into NP rats, carotid catheters were inserted on day 18, and on day 19, mean arterial pressure (MAP) was recorded, serum and plasma were collected, and oxidative stress and production of agonistic autoantibodies to the ANG II type I receptor (AT<jats:sub>1<\/jats:sub>-AA) were analyzed. MAP increased from 100.3 \u00b1 1.7 mmHg in normal pregnant (NP; n = 17) to 124.8 \u00b1 2.1 mmHg in RUPP ( n = 22; P &lt; 0.0001) and to 110.8 \u00b1 2.8 mmHg in NP+RUPP T<jats:sub>H<\/jats:sub>17 ( n = 11). Pup weights in NP+RUPP T<jats:sub>H<\/jats:sub>17s were decreased to 1.92 \u00b1 0.09 g from 2.39 \u00b1 0.14 in NP rats ( P &lt; 0.01). AT<jats:sub>1<\/jats:sub>-AA significantly increased from 0.1 \u00b1 0.2 beats\/min in NP to 15.6 \u00b1 0.7 beats\/min in NP+RUPP T<jats:sub>H<\/jats:sub>17s. IL-6 was 22.3 \u00b1 5.7 pg\/ml in NP and increased to 60.45 \u00b1 13.8 pg\/ml in RUPP ( P &lt; 0.05) and 75.9 \u00b1 6.8 pg\/ml in NP+RUPP T<jats:sub>H<\/jats:sub>17 rats ( P &lt; 0.01). Placental and renal oxidative stress were 238 \u00b1 27.5 and 411 \u00b1 129.9 relative light units\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b7mg<jats:sup>\u22121<\/jats:sup> in NP and 339 \u00b1 104.6 and 833 \u00b1 331.1 relative light units\u00b7min<jats:sup>\u22121<\/jats:sup>\u00b7mg<jats:sup>\u22121<\/jats:sup> in NP+RUPP T<jats:sub>H<\/jats:sub>17, respectively. In conclusion, RUPP T<jats:sub>H<\/jats:sub>17 cells induced intrauterine growth restriction and increased blood pressure, AT<jats:sub>1<\/jats:sub>-AA, IL-6, and tissue oxidative stress when transferred to NP rats, indicating a role for autoimmune associated T<jats:sub>H<\/jats:sub>17 cells, to cause much of the pathophysiology associated with preeclampsia. <\/jats:p>","DOI":"10.1152\/ajpregu.00117.2016","type":"journal-article","created":{"date-parts":[[2016,10,26]],"date-time":"2016-10-26T23:19:32Z","timestamp":1477523972000},"page":"R1192-R1199","source":"Crossref","is-referenced-by-count":67,"title":["Reduced uterine perfusion pressure T-helper 17 cells cause pathophysiology associated with preeclampsia during pregnancy"],"prefix":"10.1152","volume":"311","author":[{"given":"Denise C.","family":"Cornelius","sequence":"first","affiliation":[{"name":"Department of Emergency Medicine, University of Mississippi Medical Center, Jackson, Mississippi;"},{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lorena M.","family":"Amaral","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kedra","family":"Wallace","sequence":"additional","affiliation":[{"name":"Department of Obstetrics and Gynecology, University of Mississippi Medical Center, Jackson, Mississippi;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nathan","family":"Campbell","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexia J.","family":"Thomas","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeremy","family":"Scott","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Florian","family":"Herse","sequence":"additional","affiliation":[{"name":"Experimental and Clinical Research Center, Max-Delbrueck Center for Molecular Medicine in the Helmholtz Association and the Charit\u00e9 Medical Faculty, Berlin, Germany; 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