作者: Takeshi Kuwata , I-Ming Wang , Tomohiko Tamura , Roshini M. Ponnamperuma , Rachel Levine
DOI: 10.1182/BLOOD.V95.11.3349.011K46_3349_3356
关键词: Myeloid 、 Cell growth 、 Myeloproliferative Disorders 、 Bone marrow 、 Endocrinology 、 Retinoic acid 、 Vitamin 、 Vitamin A deficiency 、 Internal medicine 、 Population 、 Biology
摘要: To examine the role of retinoids in hematopoietic cell growth vivo, we studied female SENCAR mice made vitamin A deficient by dietary restriction. Deficient exhibited a dramatic increase myeloid cells bone marrow, spleen, and peripheral blood. The abnormal expansion was detected from an early stage deficiency contrasted with essentially normal profiles T B lymphocytes. This abnormality reversed on addition retinoic acid to A-deficient diet, indicating that is direct result deficiency. TUNEL analysis indicated spontaneous apoptosis, process life cycle cells, impaired mice, which may play increased population. Quantitative reverse transcriptase-polymerase chain reaction purified granulocytes showed expression not only RAR, but RXRs, 2 nuclear receptors mediate biologic activities retinoids, significantly reduced mice. work shows critically control homeostasis population vivo suggests this signaling pathway contribute various myeloproliferative disorders.