Smad‑binding decoy reduces extracellular matrix expression in human hypertrophic scar fibroblasts
- Chen Fan
- Samir El Andaloussi
- Taavi Lehto
- Kiat Whye Kong
- Yiqi Seow
Affiliations: Skin Research Institute of Singapore, Agency for Science, Technology and Research (A STAR), Singapore 138648, Republic of Singapore, Department of Laboratory Medicine, Center for Advanced Therapies, Karolinska Institute, Stockholm 14186, Sweden, Molecular Engineering Laboratory, Institute of Bioengineering and Nanotechnology, A STAR, Singapore 138669, Republic of Singapore
- Published online on: September 29, 2020 https://doi.org/10.3892/mmr.2020.11549
Copyright: © Fan
et al. This is an open access article distributed under the
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The exact mechanisms underlying hypertrophic scarring is yet to be fully understood. However, excessive collagen deposition by fibroblasts has been demonstrated to result in hypertrophic scar formation, and collagen synthesis in dermal fibroblasts is regulated by the transforming growth factor‑β1/Smad signaling pathway. In view of this, a Smad‑binding decoy was designed and its effects on hypertrophic scar‑derived human skin fibroblasts was evaluated. The results of the present study revealed that the Smad decoy attenuates the total amount of collagen, collagen I and Smad2/3 expression in scar fibroblasts. Data from RNA sequencing indicated that the Smad decoy induced more than 4‑fold change in 178 genes, primarily associated with to the extracellular matrix, compared with the untreated control. In addition, results from quantitative real‑time polymerase chain reaction further confirmed that the Smad decoy significantly attenuated the expression of extracellular matrix‑related genes, including COL1A1, COL1A2 and COL3A1. Furthermore, the Smad decoy reduced transforming growth factor‑β1‑induced collagen deposition in scar fibroblasts. Data generated from the present study provide evidence supporting the use of the Smad decoy as a potential hypertrophic scar treatment.