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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
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Visualization and Quantification of Mesenchymal Cell Adipogenic Differentiation Potential with a Lineage Specific Marker
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Fibrillin-1 Inhibits Early Adipogenic Commitment Via αvβ3 Integrin Signaling.

Iram Fatima S Siddiqui1, Valentin Nelea2, Kerstin Tiedemann1

  • 1Faculty of Medicine and Health Sciences, Department of Anatomy and Cell Biology, McGill University, Montreal, QC, Canada.

Journal of Molecular Biology
|June 16, 2026
PubMed
Summary
This summary is machine-generated.

Extracellular fibrillin-1 limits fat cell differentiation by engaging integrin αvβ3. This interaction activates a signaling cascade that suppresses adipogenesis, revealing a new mechanism for controlling adiposity.

Keywords:
RGD motifadipogenesisextracellular matrixfibrillin-1integrins

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Molecular Biology

Background:

  • Fibrillin-1 is crucial for connective tissues and its mutations cause Marfan syndrome.
  • Fibrillin-1 deficiency is linked to obesity, particularly in older individuals, by affecting adipogenic stem cell differentiation.
  • The specific cell receptors and signaling pathways involved in fibrillin-1's regulation of adipogenesis were previously unknown.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which fibrillin-1 influences adipogenic differentiation.
  • To identify the cell surface receptors and downstream signaling cascades involved in fibrillin-1's anti-adipogenic effects.
  • To investigate the role of integrin binding motifs in fibrillin-1's function during early adipogenesis.

Main Methods:

  • Used recombinant fibrillin-1 fragments with active (RGD) or inactive (RGA) integrin-binding motifs.
  • Tested the effects of these fragments on adipogenic differentiation in primary mesenchymal progenitors and 3T3-L1 cells.
  • Employed siRNA gene silencing and pharmacological inhibitors to investigate the roles of integrin αvβ3, Fak, Src, and Erk signaling pathways.

Main Results:

  • Recombinant fibrillin-1 with an active RGD motif inhibited early adipogenic differentiation, while the RGA control had no effect.
  • Inhibition of adipogenesis by fibrillin-1 required integrin αvβ3 and triggered the Fak-Src-Erk signaling cascade.
  • This cascade suppressed key adipogenic transcription factors (Cebpα and Pparγ), maintaining progenitor cell undifferentiation.
  • Inhibiting Fak, Src, or Erk rescued the anti-adipogenic effect of fibrillin-1.

Conclusions:

  • Fibrillin-1 negatively regulates early adipogenic differentiation through engagement of integrin αvβ3.
  • The integrin αvβ3-Fak-Src-Erk signaling axis acts as a critical checkpoint, limiting excessive adipogenesis.
  • This pathway provides a novel molecular explanation for fibrillin-1's role in adiposity regulation and Marfan syndrome phenotypes.