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Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
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Expression of TGF-β1/mTOR signaling pathway in pathological scar fibroblasts

Xiao-Xiang Zhai1, Zhi-Ming Tang1, Ji-Cun Ding2

  • 1Department of Dermatology, Traditional Chinese Medicine Hospital of Xuzhou City, Xuzhou, Jiangsu 221003, P.R. China.

Molecular Medicine Reports
|April 11, 2017
PubMed

Insights

Pathological scar fibroblasts show increased expression of key molecules in the transforming growth factor-β1/mammalian target of rapamycin (TGF-β1/mTOR) pathway. This heightened pathway activity is a potential mechanism driving pathological scar formation.

Area of Science:

  • Cell Biology
  • Dermatology
  • Molecular Biology

Background:

  • Pathological scars result from aberrant fibroblast activity.
  • Understanding the molecular mechanisms of scar formation is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the expression of key molecules within the transforming growth factor-β1/mammalian target of rapamycin (TGF-β1/mTOR) pathway in pathological scar fibroblasts.
  • To determine if this pathway is upregulated in scar tissue compared to normal skin.

Main Methods:

  • Utilized immunofluorescence to visualize protein expression.
  • Employed reverse transcription-polymerase chain reaction (RT-PCR) for mRNA analysis.
  • Conducted western blot analysis to quantify protein levels of TGF-β1, PI3K, Akt, and mTOR.

Main Results:

  • Immunofluorescence revealed significantly enhanced TGF-β1, PI3K, and Akt expression in pathological scar fibroblasts, primarily in the cell nucleus.
  • RT-PCR and western blot confirmed significantly higher mRNA and protein levels of TGF-β1, PI3K, Akt, and mTOR in pathological scar fibroblasts compared to normal skin fibroblasts.
  • Demonstrated a significant increase in the expression of the TGF-β1/mTOR signaling pathway in pathological scar fibroblasts.

Conclusions:

  • The TGF-β1/mTOR signaling pathway is significantly upregulated in pathological scar fibroblasts.
  • This enhanced pathway expression is a potential key mechanism contributing to the development of pathological scars.

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