title: Lamin expression in human adipose cells in relation to anatomical site and differentiation state.
abstract: Familial partial lipodystrophy-Dunnigan variety (FPLD) is an autosomal dominant form of lipodystrophy resulting in a loss of sc fat from the trunk and limbs with retention of fat in the visceral depots, face, and neck. Specific point mutations in the gene encoding the nuclear lamina proteins, lamins A and C, have been established to cause this syndrome. We undertook studies to determine which members of the lamin family were expressed in human fat cells, to examine the effect of differentiation state on lamin A and C expression in human preadipocytes, and to test the hypothesis that regional variation in lamin A/C expression might underlie the stereotyped anatomical pattern of FPLD. Lamins A, C, and B1, but not B2, were expressed in sc mature human adipocytes. Subcutaneous preadipocytes expressed all four lamins, with lamin A and C expression increasing with ex vivo differentiation. Consistent with previously reported resistance to ex vivo differentiation, omental preadipocytes did not show an increase in lamin A or C mRNA under these conditions. Lamin A/C mRNA levels were similar in isolated mature adipocytes and preadipocytes from omental, sc, and neck sites. However, lamin C was consistently lower, and the ratio of lamin A/C mRNA was higher in sc mature adipocytes compared with omental mature adipocytes. We conclude that the depot-specific pattern of lamin A/C expression does not provide clues to the mechanism of FPLD. Nonetheless, these studies provide new information regarding the expression of lamin isoforms in normal human adipose cells, which will inform future studies of the molecular pathogenesis of FPLD.
authors.affiliation: Department of Clinical Biochemistry, University of Cambridge, Addenbrooke's Hospital, Hills Road, Cambridge, CB2 2QQ, United Kingdom.
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Lelliott
authors.forename: Lisa
authors.initials: L
authors.lastname: Logie
authors.forename: Ciaran P
authors.initials: CP
authors.lastname: Sewter
authors.forename: Dirk
authors.initials: D
authors.lastname: Berger
authors.forename: Piyush
authors.initials: P
authors.lastname: Jani
authors.forename: Fiona
authors.initials: F
authors.lastname: Blows
authors.forename: Stephen
authors.initials: S
authors.lastname: O'Rahilly
authors.forename: Antonio
authors.initials: A
authors.lastname: Vidal-Puig
mesh_terms: D017667:Adipocytes / Q000166:cytology* / Q000378:metabolism* / Q000502:physiology; D002454:Cell Differentiation / Q000502:physiology; D002478:Cells, Cultured; D016922:Cellular Senescence / Q000502:physiology; D005260:Female; D006801:Humans; D034904:Lamin Type A; D034921:Lamin Type B; D007797:Laminin / Q000235:genetics / Q000378:metabolism*; D034882:Lamins; D008297:Male; D009333:Neck; D009687:Nuclear Proteins / Q000235:genetics / Q000378:metabolism*; D009852:Omentum; D012333:RNA, Messenger / Q000378:metabolism; D012867:Skin; D013234:Stem Cells / Q000166:cytology / Q000378:metabolism
chemical_list: D034904:Lamin Type A; D034921:Lamin Type B; D007797:Laminin; D034882:Lamins; D009687:Nuclear Proteins; D012333:RNA, Messenger; C440308:lamin C; C084098:laminin A