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Related Experiment Video

Updated: Jan 8, 2026

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
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TSP2 Deficiency Promotes Fibroblast Proliferation and Migration With Enhanced WNT4/β-Catenin/TGFb3.

Yaqing Huang1,2, Hao Xing2,3, Jingru Tian4

  • 1Department of Pathology, Yale University, New Haven, Connecticut, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|December 22, 2025
PubMed
Summary

Removing Thrombospondin-2 (TSP2) enhances fibroblast function, promoting tissue repair. TSP2 deficiency upregulates key regenerative pathways, suggesting it as a therapeutic target for chronic wounds.

Keywords:
Wnt/β‐cateninextracellular matrixfibroblaststhrombospondin‐2transforming growth factor beta

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Area of Science:

  • Cell Biology
  • Wound Healing Research
  • Biochemistry

Background:

  • Chronic wounds represent a significant healthcare challenge due to impaired fibroblast function and extracellular matrix (ECM) remodeling.
  • Thrombospondin-2 (TSP2), a matricellular glycoprotein, is known to impede wound healing processes.

Purpose of the Study:

  • To investigate the cellular and transcriptomic effects of TSP2 deficiency in dermal fibroblasts.
  • To elucidate the role of TSP2 in regulating fibroblast behavior and ECM interactions during tissue repair.

Main Methods:

  • Bulk RNA sequencing was performed on wild-type (WT) and TSP2 knockout (TSP2 KO) murine primary fibroblasts.
  • CRISPR/Cas9 gene editing was used to create a stable TSP2 knockout in NIH3T3 fibroblasts for robust model validation.

Main Results:

  • TSP2 deficiency led to the upregulation of pro-regenerative molecules and signaling pathways, including TGF-β3 and Wnt4/β-catenin.
  • TSP2 depletion enhanced fibroblast proliferation and migration in the engineered cell model.
  • Increased activity of TGF-β3 and Wnt/β-catenin signaling pathways was observed in TSP2-deficient fibroblasts.

Conclusions:

  • TSP2 negatively regulates fibroblast function and ECM remodeling, impacting wound healing.
  • Targeting TSP2 presents a potential therapeutic strategy for enhancing regeneration in chronic and impaired wound healing.