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Chemically Modified SDF-1α mRNA Promotes Random Flap Survival by Activating the SDF-1α/CXCR4 Axis in Rats.

Zucheng Luo1,2,3, Yujie Bian1,2,3, Gang Zheng1,2,3

  • 1Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China.

Frontiers in Cell and Developmental Biology
|February 22, 2021
PubMed
Summary
This summary is machine-generated.

Engineered fibroblasts expressing modified mRNA for stromal cell-derived factor-1α (SDF-1α) can salvage ischemic random skin flaps. This approach significantly reduces tissue necrosis and enhances vascularization, offering a promising regenerative strategy.

Keywords:
SDF-1αSDF-1α/CXCR4modRNArandom skin flapregeneration

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Area of Science:

  • Regenerative Medicine
  • Plastic and Reconstructive Surgery
  • Molecular Therapy

Background:

  • Random skin flaps are crucial in reconstructive surgery but face challenges like ischemia and necrosis.
  • Chemically modified messenger RNA (modRNA) shows significant therapeutic potential.
  • Improving blood supply and tissue survival in random skin flaps is a clinical need.

Purpose of the Study:

  • To investigate the efficacy of fibroblasts engineered with SDF-1α modRNA for random skin flap survival.
  • To evaluate the impact of this therapy on neovascularization and tissue necrosis.
  • To elucidate the underlying molecular mechanisms, including signaling pathway activation.

Main Methods:

  • Fibroblasts were engineered to express modified mRNA encoding stromal cell-derived factor-1α (SDF-1α).
  • These engineered fibroblasts were applied to random skin flaps in an experimental model.
  • Tissue necrosis, neovascularization, and key intracellular signaling pathways (SDF-1α/CXCR4, MEK/ERK, PI3K/AKT, JAK2/STAT3) were analyzed.

Main Results:

  • Fibroblast SDF-1α modRNA treatment significantly reduced tissue necrosis in random skin flaps.
  • Neovascularization was markedly promoted in the treated flaps compared to control and vehicle groups.
  • modRNA expression activated the SDF-1α/CXCR4 pathway while inactivating MEK/ERK, PI3K/AKT, and JAK2/STAT3 pathways.

Conclusions:

  • Fibroblast-mediated SDF-1α modRNA expression is a potent strategy for salvaging ischemic random skin flaps.
  • This approach enhances flap survival by promoting neovascularization and reducing necrosis.
  • The therapy's mechanism involves modulation of specific cell signaling pathways crucial for proliferation and migration.