Smad‑binding decoy reduces extracellular matrix expression in human hypertrophic scar fibroblasts

Smad‑binding decoy reduces extracellular matrix expression in human hypertrophic scar fibroblasts
Title:
Smad‑binding decoy reduces extracellular matrix expression in human hypertrophic scar fibroblasts
Other Titles:
Medicine Reports
Keywords:
Publication Date:
29 September 2020
Citation:
Fan, C., El Andaloussi, S., Lehto, T., Kong, K.W., & Seow, Y. (2020). Smad‑binding decoy reduces extracellular matrix expression in human hypertrophic scar fibroblasts. Molecular Medicine Reports, 22, 4589-4600. https://doi.org/10.3892/mmr.2020.11549
Abstract:
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.
License type:
http://creativecommons.org/licenses/by-nc-nd/4.0/
Funding Info:
This work was funded by core funding for the Molecular Engineering Laboratory and the Molecular Therapeutics Programme grant (grant no. IA F‑PP/H17/01/a0/012) and Wound Care Innovation for the Tropics [grant no. IA F‑PP/2017 (HBMS) H17/01/a0/009].
Description:
ISSN:
1791-2997
1791-3004
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