PhotoBioModulation
Wound Healing & Burns
Wound Healing
Burn Wound Healing
PubMed | PMID: 32231809 PMCID: PMC7091526 DOI:
Accelerated burn wound healing with photobiomodulation therapy involves activation of endogenous latent TGF-β1
Accelerated burn wound healing with photobiomodulation therapy involves activation of endogenous latent TGF-β1
Accelerated burn wound healing with photobiomodulation therapy involves activation of endogenous latent TGF-β1
★ Key Take-Aways
⮕ PBM treated burn wounds had significantly improved burn wound healing compared to controls (p < 0.05) (Fig. 1f, g).
⮕ These observations indicate that a non-invasive, low-dose biophotonics treatment could be effectively used in burn wound management.
Authors
Imran Khan, Saeed Ur Rahman, Elieza Tang, Karl Engel, Bradford Hall, Ashok B. Kulkarni & Praveen R. Arany
The severity of tissue injury in burn wounds from associated inflammatory and
immune sequelae presents a significant clinical management challenge. Among
various biophysical wound management approaches, low dose biophotonics
treatments, termed Photobiomodulation (PBM) therapy, has gained recent attention.
One of the PBM molecular mechanisms of PBM treatments involves photoactivation of latent TGF-β1 that is capable of promoting tissue healing and regeneration.
This work examined the efficacy of PBM treatments in a full-thickness burn wound healing
in C57BL/6 mice. We first optimized the PBM protocol by monitoring tissue surface
temperature and histology. We noted this dynamic irradiance surface temperature monitored PBM protocol improved burn wound healing in mice with elevated TGF-β
signaling (phospho-Smad2) and reduced inflammation-associated gene expression.
Next, we investigated the roles of individual cell types involved in burn wound healing
following PBM treatments and noted discrete effects on epithelieum, fibroblasts, and
macrophage functions. These responses appear to be mediated via both TGF-β dependent and independent signaling pathways.
Finally, to investigate specific contributions of TGF-β1 signaling in these PBM-burn wound healing, we utilized a chimeric TGF-β1/β3 knock-in (TGF-β1 ) mice. PBM treatments failed to activate the chimeric TGF-β1 complex and failed to improve burn wound healing in these mice.
These results suggest activation of endogenous latent TGF-β1 following PBM treatments plays a key role in burn wound healing.
These mechanistic insights can improve the safety and efficacy of clinical translation of PBM treatments for tissue healing and regeneration.
PubMed Central | PMID: 34183697 PMCID: PMC8238984 DOI: 10.1038/s41598-021-92650-w