hTERT-immortalized adipose-derived stem cell line ASC52Telo demonstrates limited potential for adipose biology

D Masnikov1, I Stafeev2, S Michurina3

  • 1Department of Angiogenesis, National Medical Research Centre for Cardiology, Moscow, Russia; Center of Master's Programs, I.M.Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University), Moscow, Russia.

Insights

Human adipose-derived stem cells (ADSC) and their immortalized counterpart ASC52Telo were compared. ASC52Telo cells show impaired adipogenesis and insulin sensitivity, making them less suitable for studying obesity and insulin resistance.

Area of Science:

  • Biomedical Science
  • Cell Biology
  • Metabolic Research

Background:

  • Obesity and insulin resistance significantly impact mortality, necessitating effective cell models for research.
  • Current models like 3T3-L1 are mouse-derived, limiting direct translation to human studies.
  • There is a critical need for relevant and renewable human adipocyte models.

Purpose of the Study:

  • To compare the adipogenic differentiation and insulin sensitivity of primary human adipose-derived stem cells (ADSC) with an immortalized ADSC cell line (ASC52Telo).
  • To evaluate the suitability of ASC52Telo as a model for studying adipocyte biology, particularly in the context of metabolic diseases.

Main Methods:

  • Flow cytometry was used to verify the mesenchymal stem cell phenotype of both ADSC and ASC52Telo.
  • Adipogenic differentiation was induced in both cell types.
  • Key adipogenic markers (FABP4, PPARg) and insulin signaling pathways (IRS1, AS160 phosphorylation) were analyzed.
  • Insulin-stimulated glucose uptake was measured.

Main Results:

  • Both ADSC and ASC52Telo exhibited a mesenchymal stem cell phenotype.
  • ASC52Telo-derived adipocytes showed reduced adipogenic differentiation efficiency compared to ADSC-derived adipocytes.
  • Insulin-stimulated glucose uptake and key protein expressions (FABP4, PPARg) were lower in ASC52Telo-derived adipocytes.
  • Impaired insulin signaling, evidenced by reduced IRS1 and AS160 phosphorylation, was observed in ASC52Telo-derived cells.

Conclusions:

  • The immortalized human ADSC line ASC52Telo retains a mesenchymal stem cell phenotype but demonstrates compromised adipogenesis.
  • ASC52Telo-derived adipocytes exhibit significantly reduced insulin sensitivity compared to primary ADSC-derived adipocytes.
  • The ASC52Telo cell line may not be an optimal model for accurately studying human adipocyte function and insulin sensitivity in metabolic research.

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