A new human adipocyte model with PTEN haploinsufficiency

Adipocyte. 2020 Dec;9(1):290-301. doi: 10.1080/21623945.2020.1785083.

Abstract

Few human cell strains are suitable and readily available as in vitro adipocyte models. We used resected lipoma tissue from a patient with germline phosphatase and tensin homolog (PTEN) haploinsufficiency to establish a preadipocyte cell strain termed LipPD1 and aimed to characterize cellular functions and signalling pathway alterations in comparison to the established adipocyte model Simpson-Golabi-Behmel-Syndrome (SGBS) and to primary stromal-vascular fraction cells. We found that both cellular life span and the capacity for adipocyte differentiation as well as adipocyte-specific functions were preserved in LipPD1 and comparable to SGBS adipocytes. Basal and growth factor-stimulated activation of the PI3 K/AKT signalling pathway was increased in LipPD1 preadipocytes, corresponding to reduced PTEN levels in comparison to SGBS cells. Altogether, LipPD1 cells are a novel primary cell model with a defined genetic lesion suitable for the study of adipocyte biology.

Keywords: 3D culture; AKT; Lipoma; SGBS; adipocyte differentiation; cellular life-span; phosphatases; phosphoinositide-3-kinase.

MeSH terms

  • Adipocytes / cytology
  • Adipocytes / metabolism*
  • Adipogenesis / genetics
  • Adipose Tissue, White / metabolism
  • Biomarkers
  • Cell Differentiation / genetics
  • Cells, Cultured
  • Gene Expression Regulation
  • Haploinsufficiency*
  • Humans
  • Lipid Metabolism
  • Lipoma / etiology
  • Lipoma / metabolism
  • Lipoma / pathology
  • PTEN Phosphohydrolase / genetics*
  • PTEN Phosphohydrolase / metabolism
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction

Substances

  • Biomarkers
  • Proto-Oncogene Proteins c-akt
  • PTEN Phosphohydrolase
  • PTEN protein, human

Grants and funding

This project was funded by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) – 209933838 – SFB 1052 – B10. Funding was also received from the Integrated Research and Treatment Center (IFB) AdiposityDiseases Leipzig (project # AD2-7105), the German Diabetes Society and Stiftung Kinderklinik Leipzig. We acknowledge support from Leipzig University for Open Access Publishing.