Dynamic biological changes in fibroblasts during hypertrophic scar formation and regression

Qing, Chun; Wang, Zhiyong; Song, Fei; Wang, Xiqiao

doi:10.1111/iwj.12283

Cited by 54 publications

(45 citation statements)

References 18 publications

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“…VEGF is an essential factor in the angiogenetic response in hypertrophic scar management. The expression of VEGF increases in early scars, peaks in proliferative scars and decreases in regressive scars [22]. Anti-Vascular Endothelial Growth Factor (Bevacizumab) therapy could reduce hypertrophic scar formation in a rabbit ear wounding model [23].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of LncRNA AC067945.2 Down-Regulates Collagen Expression in Skin Fibroblasts and Possibly Correlates with the VEGF and Wnt Signalling Pathways

Chen¹,

Li²,

Li³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Long non-coding RNAs (lncRNAs) are thought to play crucial roles in human diseases. However, the function of lncRNAs in hypertrophic scar formation remains poorly understood. Methods: Utilizing qRT-PCR, we explored the expression changes of AC067945.2. Overexpression of AC067945.2 in normal skin fibroblasts was performed by transient plasmid transfection. Western blot was used to check the proteins' expression changes. Cell Counting Kit-8 (CCK-8) assay and Annexin V/7-AAD staining were used to examine cell proliferation and apoptosis, respectively. mRNA-seq was applied to dissect the differentially expressed mRNAs in AC067945.2 overexpressed cells. We also performed ELISA to detect the VEGF secretion. Results: AC067945.2 was down-regulated in hypertrophic scar tissues. Overexpression of AC067945.2 did not affect cell proliferation, but it mildly promoted early apoptosis in normal skin fibroblasts. Furthermore, AC067945.2 overexpression inhibited the expression of COL1A1, COL1A2, COL3A1 and α-SMA proteins. Transforming growth factor-β1 (TGF-β1) could inhibit the expression of AC067945.2. Based on mRNA-seq data, compared with mRNAs in the control group, 138 mRNAs were differentially expressed, including 14 upregulated and 124 down-regulated transcripts, in the AC067945.2 overexpression group. Gene ontology and pathway analyses revealed that AC067945.2 overexpression was correlated with developmental processes, binding, extracellular region, and the vascular endothelial

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Section: Discussionmentioning

confidence: 99%

Overexpression of LncRNA AC067945.2 Down-Regulates Collagen Expression in Skin Fibroblasts and Possibly Correlates with the VEGF and Wnt Signalling Pathways

Chen¹,

Li²,

Li³

et al. 2018

Cell Physiol Biochem

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“…They originate from a process of activation and transdifferentiation mainly involving the monocyte lineage, mesenchymal stem cells and circulating fibrocytes. The switch from PMF to MF is possibly related to TGF-β1 produced by a large set of cell types involved in wound healing [17,18,19]. Natural resolution of abnormal scarring possibly follows the complete epithelialization.…”

Section: Discussionmentioning

confidence: 99%

“…Switching PMF to mature MF probably relies on the effect of transforming growth factor-β1 (TGF-β1) produced and released by a series of inflammatory cells, and possibly by fibroblast-like cells [17,18,19]. Thus, MF differentiation is regulated by the combination of specific cells and a series of ECM molecular components [20,21,22].…”

Section: Introductionmentioning

confidence: 99%

Protomyofibroblast Pathway in Early Thermal Burn Healing

Hermanns‐Lê

Pierard

Jennes

et al. 2015

Skin Pharmacol Physiol

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Wound healing following partial thickness thermal burns is commonly hampered by the risk of hypertrophic scarring. Skin myofibroblast (MF) density is commonly increased in postburn healing. The transition between fibroblast-like cells and α-smooth muscle actin (SMA)+ MF possibly begins with CD14+ monocytes, evolving to CD14+ CD34+ fibrocytes, followed by β-SMA+ protomyofibroblast (PMF) maturation. Skin biopsies from 25 burn patients were collected about 1 and 4 weeks after injury. Immunohistochemistry was performed using monoclonal antibodies to α-SMA, β-SMA, factor XIIIa, lysozyme, Mac 387, CD14, CD117 and Ulex europaeus agglutinin-1 (UEA-1). The set of Mac 387+ and CD14+ monocytes was accompanied by both CD34+ fibrocytes and factor XIIIa+ dendrocytes. By contrast, β-SMA+ PMF were rare. Of note, α-SMA+ MF were more abundant at week 4 than at week 1 (p < 0.01). The UEA-1+ endothelial cells showed marked variations in their dermal distribution, irrespective of the densities in the other scrutinized cells. In conclusion, healing of partial thickness thermal burns involves a diversity of cell types including PMF. In the present samples, the PMF density remained low.

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“…Fibroblasts are spindle-shaped cells, and initially appear at the location of injury at the end of the inflammatory phase and beginning of the proliferative phase of healing wound [4]. Commonly, fibroblasts are activated and differentiate into myofibroblasts, which are a phenotypically intermediate cell type between fibroblasts and smooth muscle cells.…”

Section: Cellular Basis Of Hypertrophic Scarsmentioning

confidence: 99%

“…Hypertrophic scars have been shown to express high levels of VEGF [82,83], and the skin biopsies of human presternal wound healing had higher microvessel densities postoperatively concomitant with upregulation of VEGF [84]. Moreover, VEGF was dynamically correlated with the progression of hypertrophic scars, because VEGF expression was increased in early scars, peaked in proliferative scars and decreased in regressive scars [4]. In addition, mast cells that contain tryptase exhibited moderate expression of VEGF in hypertrophic and surgical scars in patients with active scar lesions [85].…”

Section: Vascular Endothelial Growth Factor Pathwaymentioning

confidence: 99%

Growth factor pathways in hypertrophic scars: Molecular pathogenesis and therapeutic implications

Lian

2016

Biomedicine & Pharmacotherapy

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Dynamic biological changes in fibroblasts during hypertrophic scar formation and regression

Cited by 54 publications

References 18 publications

Overexpression of LncRNA AC067945.2 Down-Regulates Collagen Expression in Skin Fibroblasts and Possibly Correlates with the VEGF and Wnt Signalling Pathways

Overexpression of LncRNA AC067945.2 Down-Regulates Collagen Expression in Skin Fibroblasts and Possibly Correlates with the VEGF and Wnt Signalling Pathways

Protomyofibroblast Pathway in Early Thermal Burn Healing

Growth factor pathways in hypertrophic scars: Molecular pathogenesis and therapeutic implications

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