Regulation of preadipocyte factor-1 gene expression during 3T3-L1 cell differentiation

Endocrinology. 1996 Jul;137(7):2923-8. doi: 10.1210/endo.137.7.8770915.

Abstract

Preadipocyte factor-1 (Pref-1), a novel gene product isolated from murine preadipocyte 3T3-L1 cells, is thought to function as a negative regulator of adipocyte differentiation. We investigated the regulation of Pref-1 expression in 3T3-L1 preadipocytes during proliferation, growth arrest, and early differentiation in the presence and absence of three well described differentiation antagonists: interleukin-11 (IL-11), transforming growth factor-beta, and tumor necrosis factor-alpha. Northern blot analysis was used to determine messenger RNA (mRNA) steady state expression of Pref-1 and two differentiation-specific genes, adipsin and glycerol-3-phosphate dehydrogenase. We confirmed that Pref-1 mRNA is abundant in proliferating preadipocytes and that its expression is dramatically reduced early in differentiation. However, proliferating and growth-arrested cells treated with the differentiation inhibitor IL-11 demonstrated a modest decrease in Pref-1 mRNA abundance. Transforming growth factor-beta and tumor necrosis factor-alpha had little effect. The reduction of Pref-1 mRNA was most dramatic in differentiating preadipocytes treated with IL-11, occurring despite inhibition of adipogenesis, as judged by cell morphology and adipocyte-specific gene expression (adipsin and glycerol-3-phosphate dehydrogenase). This effect of IL-11 on Pref-1 suggests that different mechanisms are responsible for the IL-11-induced and the differentiation- associated down-regulation of Pref-1, thus dissociating Pref-1 regulation from differentiation. We conclude that Pref-1 expression is not a reliable marker of preadipocytes, and that decreased Pref-1 abundance does not function as a trigger for adipocyte differentiation.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 1-Methyl-3-isobutylxanthine / pharmacology
  • 3T3 Cells
  • Adipocytes / cytology*
  • Adipocytes / metabolism
  • Animals
  • Base Sequence
  • Blotting, Northern
  • Calcium-Binding Proteins
  • Cell Differentiation*
  • Cell Division / drug effects
  • Complement Factor D
  • DNA Primers
  • DNA, Complementary
  • Dexamethasone / pharmacology
  • Gene Expression Regulation* / drug effects
  • Glycerolphosphate Dehydrogenase / biosynthesis
  • Insulin / pharmacology
  • Intercellular Signaling Peptides and Proteins
  • Interleukin-1 / pharmacology
  • Kinetics
  • Membrane Proteins / biosynthesis*
  • Mice
  • Molecular Sequence Data
  • Polymerase Chain Reaction
  • RNA, Messenger / metabolism
  • Repressor Proteins / biosynthesis*
  • Serine Endopeptidases / biosynthesis
  • Transcription, Genetic / drug effects
  • Transforming Growth Factor beta / pharmacology
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Calcium-Binding Proteins
  • DNA Primers
  • DNA, Complementary
  • Dlk1 protein, mouse
  • Insulin
  • Intercellular Signaling Peptides and Proteins
  • Interleukin-1
  • Membrane Proteins
  • RNA, Messenger
  • Repressor Proteins
  • Transforming Growth Factor beta
  • Tumor Necrosis Factor-alpha
  • Dexamethasone
  • Glycerolphosphate Dehydrogenase
  • Serine Endopeptidases
  • Complement Factor D
  • complement factor D, mouse
  • 1-Methyl-3-isobutylxanthine