{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T02:32:38Z","timestamp":1790303558697,"version":"4.1.0"},"reference-count":44,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Endocrinology and Metabolism"],"published-print":{"date-parts":[[2002,5,1]]},"abstract":"<jats:p>We have shown that leukemia inhibitory factor (LIF) and suppressor of cytokine signaling (SOCS)-3 are expressed in the hypothalamus and pituitary and that LIF induces proopiomelanocortin (POMC) and ACTH, whereas SOCS-3 abrogates corticotroph POMC gene transcription and ACTH secretion. Here, we determined the role of pituitary LIF and SOCS-3 in regulating hypothalamo-pituitary-adrenal (HPA) axis inflammatory responses. Murine pituitary LIF expression was induced up to eightfold after intraperitoneal injection of lipopolysaccharide or tumor necrosis factor-\u03b1, concordant with elevated plasma levels of ACTH and corticosterone. In LIF knockout (LIFKO) mice, induction of both ACTH and corticosterone were attenuated. LIF deletion was associated with elevated ( P &lt; 0.05) levels of pituitary TNF-\u03b1, interleukin (IL)-1\u03b2, and IL-6 mRNA and cytokine-inducible pituitary SOCS-3 expression. Abrogation of the HPA axis stress response and higher pituitary levels of proinflammatory cytokines observed in LIFKO mice resulted in a stronger inflammatory process, as evidenced by elevated erythrocyte sedimentation rate and increased serum amyloid A levels ( P &lt; 0.05). The results indicate that, although LIF induces ACTH, SOCS-3 acts to counterregulate the HPA axis response to inflammation.<\/jats:p>","DOI":"10.1152\/ajpendo.00442.2001","type":"journal-article","created":{"date-parts":[[2015,2,27]],"date-time":"2015-02-27T20:09:24Z","timestamp":1425067764000},"page":"E1110-E1118","source":"Crossref","is-referenced-by-count":17,"title":["Opposing effects of pituitary leukemia inhibitory factor and SOCS-3 on the ACTH axis response to inflammation"],"prefix":"10.1152","volume":"282","author":[{"given":"Vera","family":"Chesnokova","sequence":"first","affiliation":[{"name":"Cedars-Sinai Research Institute-University of California Los Angeles School of Medicine, Los Angeles, California 90048"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anastasia","family":"Kariagina","sequence":"additional","affiliation":[{"name":"Cedars-Sinai Research Institute-University of California Los Angeles School of Medicine, Los Angeles, California 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