title: Establishment of a human preadipose cell line, HPB-AML-I: refractory to PPARgamma-mediated adipogenic stimulation.
abstract: In this study, we established a unique cell line, HPB-AML-I (AML-I), from peripheral blood mononuclear cells collected from a patient with acute myeloid leukemia (AML: M1). Morphological and phenotypical analyses of the established AML-I cells demonstrated that they belong to a preadipocyte cell line as indicated by their storage of lipid droplets and expression of surface antigens similar to those found on bone marrow stromal cells (MSC). Through cell culture under adipogenic conditions, effective differentiation of AML-I cells into adipocytes was induced by an adipogenesis inducing cocktail (INC) made up of a mixture of methylisobutylxanthine, hydrocortisone, and indomethacin. By contrast, activation of peroxisome proliferator-activated receptor (PPARgamma), which plays a key role in lipids metabolism and is highly expressed in AML-I cells, decreased the number of lipid droplets in AML-I cells. Here we report the establishment of a unique human derived-preadipocyte cell line, AML-I, and its bi-directional adipogenic response to different type stimulation, i.e., one is a refractory response to troglitazone, a well-known adipogenic stimulator, and a positive response to INC, an adipogenesis induction cocktail. These results suggest that, based on the adipogenic response, there might be some distinct lineages in human adipocytes and that the unique differentiation of AML-I cells should be useful for analyzing both the differentiation and regulation of human preadipocytes.
authors.affiliation: Department of Pathology, 1st Unit, Shimane Medical University, Izumo, Japan. ikuko@shimane-med.ac.jp
authors.forename: Ikuko
authors.initials: I
authors.lastname: Torii
authors.forename: Shigeru
authors.initials: S
authors.lastname: Morikawa
authors.forename: Akinobu
authors.initials: A
authors.lastname: Nakano
authors.forename: Keiko
authors.initials: K
authors.lastname: Morikawa
mesh_terms: D017667:Adipocytes / Q000166:cytology* / Q000502:physiology; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D015703:Antigens, CD / Q000096:biosynthesis; D000970:Antineoplastic Agents / Q000494:pharmacology; D002454:Cell Differentiation / Q000187:drug effects* / Q000502:physiology*; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D002839:Chromans / Q000494:pharmacology; D005434:Flow Cytometry; D005455:Fluorescent Antibody Technique; D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology; D007150:Immunohistochemistry; D002479:Inclusion Bodies / Q000648:ultrastructure; D007213:Indomethacin / Q000494:pharmacology; D015470:Leukemia, Myeloid, Acute / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000166:cytology; D008854:Microscopy, Electron; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism*; D013844:Thiazoles / Q000494:pharmacology; D045162:Thiazolidinediones; D014157:Transcription Factors / Q000378:metabolism*; D000077288:Troglitazone
chemical_list: D000893:Anti-Inflammatory Agents; D000894:Anti-Inflammatory Agents, Non-Steroidal; D015703:Antigens, CD; D000970:Antineoplastic Agents; D002839:Chromans; D018160:Receptors, Cytoplasmic and Nuclear; D013844:Thiazoles; D045162:Thiazolidinediones; D014157:Transcription Factors; D000077288:Troglitazone; D006854:Hydrocortisone; D007213:Indomethacin