{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,3,2]],"date-time":"2025-03-02T05:36:32Z","timestamp":1740893792052,"version":"3.38.0"},"reference-count":52,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2000,5,1]],"date-time":"2000-05-01T00:00:00Z","timestamp":957139200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Lupus"],"published-print":{"date-parts":[[2000,5]]},"abstract":"<jats:p> Estrogen is thought to contribute to the onset of systemic lupus erythematosus (SLE) in women through mechanisms that are not completely understood. Although estrogen serves as a negative regulator in normal hematopoietic development, little research has been conducted examining alteration in hematopoietic development triggered by estrogen in lupus-susceptible individuals. We examined whether estrogen and other factors could influence colony formation of bone marrow cells obtained from normal and lupus-susceptible mice. Bone marrow cells isolated from New Zealand Black (NZB) and lupus-prone New Zealand Black and New Zealand White cross (NZB\/W) mice were cultured in the presence of granulocyte-macrophage colony stimulating factor (GM-CSF) alone or in combination with estrogen, thrombopoietin (TPO), tamoxifen, estrogen and TPO, or estrogen and tamoxifen, and plated in methylcellulose culture medium. Plates were scored for the number of CFU-GM (colony forming unit granulocyte-macrophage) colonies after 6 d in culture. For females of both mouse strains, estrogen significantly decreased (P &lt; 0.05) the number of GM colonies. Co-treatment of NZB\/W cells, but not NZB cells, with TPO or tamoxifen reversed the suppressive action of estrogen (P &lt; 0.05). In contrast, while estrogen did suppress colony formation from cells of NZB\/W males (P &lt; 0.05), neither TPO nor tamoxifen reversed this effect. Our results indicate that the sensitivity of bone marrow cells isolated from both female and male NZB\/W lupus-prone mice to hormones\/growth factors is qualitatively different from cells of NZB mice, and suggest that hematopoietic alterations at the level of the bone marrow may be related to the pathogenesis of SLE. <\/jats:p>","DOI":"10.1191\/096120300680198962","type":"journal-article","created":{"date-parts":[[2003,11,12]],"date-time":"2003-11-12T12:45:16Z","timestamp":1068641116000},"page":"271-277","source":"Crossref","is-referenced-by-count":9,"title":["Altered bone marrow cell sensitivity in the lupus-prone NZB\/W mouse:                 regulation of CFU-GM colony formation by estrogen, tamoxifen and thrombopoietin"],"prefix":"10.1177","volume":"9","author":[{"given":"S M","family":"Aronica","sequence":"first","affiliation":[{"name":"Department of Biology, Canisius College, Buffalo, NY, USA; Department of                         Biology, Canisius College, 304 Health Science Center, 2001 Main Street,                         Buffalo, NY 14208, USA;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A","family":"Dozier","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P","family":"Fanti","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M","family":"Nazareth","sequence":"additional","affiliation":[{"name":"Department of Biology, Canisius College, Buffalo, NY, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2000,5,1]]},"reference":[{"key":"atypb1","first-page":"217","volume":"13","author":"Cutolo M","year":"1995","journal-title":"Clin Exp Rheumatol"},{"key":"atypb2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1998.tb09547.x"},{"key":"atypb3","doi-asserted-by":"crossref","unstructured":"Howie SEM                 ,                      Harrison DJ                 ,                      Wyllie AH                 .                      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