Wound natural healing in treatment of tumor-like hypertrophic scar

Han, Tong; Du, Lin; Jiang, Hua

doi:10.1590/abd1806-4841.20176656

Cited by 3 publications

(4 citation statements)

References 14 publications

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“…Dermal scars are the result of wound healing and remodeling. 1 Myofibroblast transdifferentiation with increased expression of α-smooth muscle actin (α-SMA) appears during the contraction stage of wound healing to reduce the surface area and facilitate reepithelialization. 2 – 4 However, distortions in this procedure or other pathological conditions can lead to the recruitment and excessive activation of myofibroblasts that lead to the formation of hypertrophic or even keloid scars.…”

mentioning

confidence: 99%

Extracellular Vesicles Derived From Human Adipose-Derived Stem Cell Prevent the Formation of Hypertrophic Scar in a Rabbit Model

Zhu

Zhang

et al. 2020

Ann Plast Surg

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Background Preventing scar formation during wound healing has important clinical implications. Numerous studies have indicated that adipose-derived stem cell culture mediums, which are rich in cytokines and extracellular vesicles (EVs), regulate matrix remodeling and prevent scar formation after wound healing. Therefore, using a rabbit scar model, we tried to demonstrate which factor in adipose-derived stem cell culture mediums plays a major role in preventing scar formation (EVs or cytokines), as well as revealing the underlying mechanism. Methods Human adipose-derived stem cells (hASCs) were isolated from the subcutaneous adipose tissue of a healthy female donor. The surface CD markers of third-passage hASCs were analyzed by flow cytometry. The adipogenic differentiation capacity of the hASCs was detected using Oil O staining. A cultured medium of third- to five-passage hASCs was collected for EV and EV-free medium isolations. Extracellular vesicles were characterized using transmission electron microscopy, NanoSight, and the Western blotting for surface markers CD63, TSG101, and Alix. The EV-free medium was characterized by Western blotting for vascular endothelial growth factor A (VEGFA), platelet derived growth factor B (PDGFB), and transforming growth factor β 1 (TGFβ1). Eight-millimeter-diameter wounds were created on the ventral side of both ears of 16 New Zealand rabbits. A total of 0.1 mL of the human adipose-derived stem cell–extracellular vesicle (hASC-EV) or EV-free medium was locally injected into wounds made on the right ears during wound healing. Meanwhile, equal amounts of phosphate buffer saline were injected into the left ears as a control. Biopsies of the wounded skin and surrounding tissue were excised on postoperative day 28 and subjected to hematoxylin and eosin (H&E), Masson, and α-SMA immunofluorescence staining. The protein expression of α-SMA and collagen I in both scar tissues and the normal skin were evaluated via Western blotting. Results The hASCs expressed high levels of 49d, CD90, CD105, and CD73 but did not express CD34 or CD45. The hASCs differentiated into adipocytes under an adipogenic induction medium. Under transmission electron microscopy, the hASC-EVs were circular, bilayer membrane vesicles and approximately 95% of the particles were between 50 and 200 nm in size. The hASC-EVs expressed the same surface markers as EVs, including CD63, TSG101, and Alix and displayed little expression of VEGFA, PDGFB, and TGFβ1. The EV-free medium had a high expression of VEGFA, PDGFB, and TGFβ1 but displayed no expression of CD63, TSG101, and Alix. In vivo, the hASC-EV treatment prevented the formation of hypertrophic scars on postoperative day 28 and suppressed collagen deposition and myofibroblast aggregation. However, the EV-free medium did not prevent the formation of hypertrophic scars on the same time point and had little effect on collagen deposition and myofibroblast aggregation when compared with the control gr...

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confidence: 99%

Extracellular Vesicles Derived From Human Adipose-Derived Stem Cell Prevent the Formation of Hypertrophic Scar in a Rabbit Model

Zhu

Zhang

et al. 2020

Ann Plast Surg

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“…During this stage, collagen type III is replaced by collagen type I to maximize strength in the wound. The increase in tensile strength may last up to a year ( Han et al, 2017 ; Wang P. H. et al, 2018 ; Lee and Jang, 2018 ).…”

Section: The Formation Process Of Hsmentioning

confidence: 99%

“…HS occurs after surgery, trauma, and especially burns. It is usually a hard and red raised scar ( Han et al, 2017 ; Le and Wu, 2021 ). HS are fibrous scars caused by abnormal skin wound healing processes and are characterized by abnormal proliferation of fibroblasts and excessive deposition of collagen ( Wang X. et al, 2018 ).…”

Section: The Formation Process Of Hsmentioning

confidence: 99%

Traditional Chinese medicine for hypertrophic scars—A review of the therapeutic methods and potential effects

Chen

Zhang

et al. 2022

Front. Pharmacol.

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Hypertrophic scar (HS) is a typical pathological response during skin injury, which can lead to pain, itching, and contracture in patients and even affect their physical and mental health. The complexity of the wound healing process leads to the formation of HS affected by many factors. Several treatments are available for HS, whereas some have more adverse reactions and can even cause new injuries with exacerbated scarring. Traditional Chinese Medicine (TCM) has a rich source, and most botanical drugs have few side effects, providing new ideas and methods for treating HS. This paper reviews the formation process of HS, the therapeutic strategy for HS, the research progress of TCM with its relevant mechanisms in the treatment of HS, and the related new drug delivery system of TCM, aiming to provide ideas for further research of botanical compounds in the treatment of HS, to promote the discovery of more efficient botanical candidates for the clinical treatment of HS, to accelerate the development of the new drug delivery system and the final clinical application, and at the same time, to promote the research on the anti-HS mechanism of multiherbal preparations (Fufang), to continuously improve the quality control and safety and effectiveness of anti-HS botanical drugs in clinical application.

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“…Therefore, strategies that reduce fibroblast proliferation and increase fibroblast apoptosis might be effective for treating HS, and it is meaningful to study the myofibroblast apoptosis [12,13]. Moreover, emerging evidences have suggested that HS have some tumor-like properties due to its excessive and rapid cell overgrowth [14]. Indeed, in recent years, emerging evidence revealed that some anticancer agents have been used as off-label treatments for HS.…”

Section: Introductionmentioning

confidence: 99%

Targeted apoptosis of myofibroblasts by elesclomol inhibits hypertrophic scar formation

Feng

Sun

et al. 2020

EBioMedicine

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Background: Hypertrophic scar (HS) is characterized by the increased proliferation and decreased apoptosis of myofibroblasts. Myofibroblasts, the main effector cells for dermal fibrosis, develop from normal fibroblasts. Thus, the stimulation of myofibroblast apoptosis is a possible treatment for HS. We aimed to explore that whether over-activated myofibroblasts can be targeted for apoptosis by anticancer drug elesclomol. Methods: 4 0 ,6-diamidino-2-phenylindole staining, flow cytometry, western blotting, collagen gel contraction and immunofluorescence assays were applied to demonstrate the proapoptotic effect of elesclomol in scar derived myofibroblasts and TGF-b1 induced myofibroblasts. The therapeutic potential of elesclomol was investigated by establishing rabbit ear hypertrophic scar models. Findings: Both 4 0 ,6-diamidino-2-phenylindole staining and flow cytometry indicated that elesclomol targets myofibroblasts in vitro. Collagen gel contraction assay showed that elesclomol inhibited myofibroblast contractility. Flow cytometry and western blot analysis revealed that elesclomol resulted in excessive intracellular levels of reactive oxygen species(ROS), and caspase-3 and cytochrome c proteins. Moreover, compared with the control group, the elesclomol group had a significantly lower scar elevation index in vivo. Immunofluorescence assays for TUNEL and a-smooth muscle actin indicated that elesclomol treatment increased the number of apoptotic myofibroblasts. Interpretation: The above results indicate that elesclomol exerted a significant inhibitory effect on HS formation via targeted myofibroblast apoptosis associated with increased oxidative stress. Thus, elesclomol is a promising candidate drug for the treatment of myofibroblast-related diseases such as HS.

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Wound natural healing in treatment of tumor-like hypertrophic scar

Cited by 3 publications

References 14 publications

Extracellular Vesicles Derived From Human Adipose-Derived Stem Cell Prevent the Formation of Hypertrophic Scar in a Rabbit Model

Extracellular Vesicles Derived From Human Adipose-Derived Stem Cell Prevent the Formation of Hypertrophic Scar in a Rabbit Model

Traditional Chinese medicine for hypertrophic scars—A review of the therapeutic methods and potential effects

Targeted apoptosis of myofibroblasts by elesclomol inhibits hypertrophic scar formation

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