Inhibition of Notch Intracellular Domain Suppresses Cell Activation and Fibrotic Factors Production in Hypertrophic Scar Fibroblasts Versus Normal Skin Fibroblasts

2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Lin Chen ◽  
Xi Zhang ◽  
Zhou Yu ◽  
Yajuan Song ◽  
Tong Wang ◽  
...  
Keyword(s):  
Hypertrophic Scar ◽  
Cell Activation ◽  
Normal Skin ◽  
Skin Fibroblasts ◽  
Intracellular Domain ◽  
Notch Intracellular Domain

Exposure to Varying Strain Magnitudes Influences the Conversion of Normal Skin Fibroblasts Into Hypertrophic Scar Cells

2016 ◽  
Vol 76 (4) ◽  
pp. 388-393 ◽  
Author(s):  
Ruixia Kuang ◽  
Zhiguo Wang ◽  
Quanchen Xu ◽  
Xia Cai ◽  
Tao Liu
Keyword(s):  
Hypertrophic Scar ◽  
Normal Skin ◽  
Skin Fibroblasts

Effects of asiaticoside on the expression of Smad protein by normal skin fibroblasts and hypertrophic scar fibroblasts

2008 ◽  
Vol 33 (2) ◽  
pp. 171-175 ◽  
Author(s):  
S. H. Qi ◽  
J.-L. Xie ◽  
S. Pan ◽  
Y.-B. Xu ◽  
T.-Z. Li ◽  
...  
Keyword(s):  
Hypertrophic Scar ◽  
Normal Skin ◽  
Skin Fibroblasts ◽  
Smad Protein

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

2018 ◽  
Vol 45 (2) ◽  
pp. 761-771 ◽  
Author(s):  
Ling Chen ◽  
Jingyun Li ◽  
Qian Li ◽  
Xue Li ◽  
Yanli Gao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Hypertrophic Scar ◽  
Normal Skin ◽  
Scar Formation ◽  
Wnt Signalling ◽  
Skin Fibroblasts ◽  
Differentially Expressed ◽  
Cell Counting ◽  
Signalling Pathways

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 up-regulated 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 cell growth factor (VEGF) and Wnt signalling pathways. ELISA confirmed that AC067945.2 overexpression could repress VEGF secretion. Conclusion: Taken together, our data uncovered the functions of a novel lncRNA AC067945.2, which might help us understand the mechanisms regulated by AC067945.2 in the pathogenesis of hypertrophic scar formation.

Fibroblasts During Hypertrophic Scar Formation and Resolution

1973 ◽  
Vol 31 ◽  
pp. 428-429
Author(s):  
C. W. Kischer
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Cell Proliferation ◽  
Fine Structure ◽  
Metabolic Activity ◽  
Hypertrophic Scar ◽  
Normal Skin ◽  
Ground Substance ◽  
Hypertrophic Scars ◽  
Scanning Electron

The morphology of the fibroblasts changes markedly as the healing period from burn wounds progresses, through development of the hypertrophic scar, to resolution of the scar by a self-limiting process of maturation or therapeutic resolution. In addition, hypertrophic scars contain an increased cell proliferation largely made up of fibroblasts. This tremendous population of fibroblasts seems congruous with the abundance of collagen and ground substance. The fine structure of these cells should reflect some aspects of the metabolic activity necessary for production of the scar, and might presage the stage of maturation.A comparison of the fine structure of the fibroblasts from normal skin, different scar types, and granulation tissue has been made by transmission (TEM) and scanning electron microscopy (SEM).

Overexpression of miR-340-5p Inhibits Skin Fibroblast Proliferation by Targeting Kruppel-like Factor 2

2019 ◽  
Vol 20 (13) ◽  
pp. 1147-1154 ◽  
Author(s):  
Ling Chen ◽  
Qian Li ◽  
Xun Lu ◽  
Xiaohua Dong ◽  
Jingyun Li
Keyword(s):  
Gene Ontology ◽  
Skin Fibroblast ◽  
Kegg Pathway ◽  
Normal Skin ◽  
Skin Fibroblasts ◽  
Differentially Expressed ◽  
Luciferase Reporter ◽  
Fibroblast Proliferation ◽  
Pathway Analyses ◽  
Normal Skin Fibroblast

<P>Objective: MicroRNA (miR)-340-5p has been identified to play a key role in several cancers. However, the function of miR-340-5p in skin fibroblasts remains largely unknown. </P><P> Methods: Gain of function experiments were performed by infecting normal skin fibroblast cells with a lentivirus carrying 22-bp miR-340-5p. Cell proliferation was detected by Cell Counting Kit-8 (CCK-8) assay. To uncover the mechanisms, mRNA-seq was used. Differentially expressed mRNAs were further determined by Gene Ontology and KEGG pathway analyses. The protein levels were analysed by Western blotting. A dual-luciferase reporter assay was used to detect the direct binding of miR-340-5p with the 3&#039;UTR of Kruppel-like factor 2 (KLF2). </P><P> Results: MiR-340-5p lentivirus infection suppressed normal skin fibroblast proliferation. The mRNAseq data revealed that 41 mRNAs were differentially expressed, including 22 upregulated and 19 downregulated transcripts in the miR-340-5p overexpression group compared with those in the control group. Gene Ontology and KEGG pathway analyses revealed that miR-340-5p overexpression correlated with the macromolecule biosynthetic process, cellular macromolecule biosynthetic process, membrane, and MAPK signalling pathway. Bioinformatics analysis and luciferase reporter assays showed that miR-340-5p binds to the 3&#039;UTR of KLF2. Forced expression of miR-340-5p decreased the expression of KLF2 in normal skin fibroblasts. Overexpression of KLF2 restored skin fibroblast proliferation in the miR-340-5p overexpression group. </P><P> Conclusion: This study demonstrates that miR-340-5p may suppress skin fibroblast proliferation, possibly through targeting KLF2. These findings could help us understand the function of miR-340-5p in skin fibroblasts. miR-340-5p could be a therapeutic target for preventing scarring.</P>

34 Rete Ridges are Decreased in Dyschromic Burn Hypertrophic Scar: A Histological Study

2021 ◽  
Vol 42 (Supplement_1) ◽  
pp. S27-S27
Author(s):  
Bonnie C Carney ◽  
Taryn E Travis ◽  
Romina Deldar ◽  
Lauren T Moffatt ◽  
Laura S Johnson ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Hypertrophic Scar ◽  
Burn Injury ◽  
Histological Study ◽  
Normal Skin ◽  
Weak Correlation ◽  
Rete Ridge ◽  
Skin Physiology ◽  
Predominantly Female ◽  
Injured Skin

Abstract Introduction Dyschromic hypertrophic scar (HTS) with areas of hyper- and hypo-pigmentation is a common sequelae of burn injury. The mechanism behind the development of dyschromia has not been elucidated. In this study, we provide a histological analysis of these scars with a focus on rete ridge presence. Rete ridges occur in epithelial tissues such as oral mucosa and skin and can be described as undulating “pegs” that are interdigitated with dermal papillae. Rete ridges enhance adhesion of the epidermis to the dermis. We hypothesize that rete ridge presence is important for normal skin physiology, and their absence or presence may hold mechanistic significance in post-burn HTS dyschromia. Methods Subjects with post-burn dyschromic HTS were consented and enrolled (n=27). Punch biopsies of hyper-, hypo-, and normally pigmented scar and skin were collected and stored in formalin. Biopsies were paraffin embedded, sectioned, stained with H&E, and imaged. The number of rete ridges were investigated by calculating a rete ridge ratio from the length of the basement membrane and the length of the epidermis. Results The patient population was predominantly female (55.5%), black (70.4%), and had Fitzpatrick skin Type V (51.9%). The injuries were primarily as a result of flame (37%) and scald (33.3%) and resulted in a median TBSA burn of 7%. The median age of the scar at the time of sample acquisition was 12.2 months. The rete ridge ratio of normally pigmented, un-injured skin was above 1 (1.31 ± 0.04), indicating that normal skin’s basement membrane is longer than its epidermal length due to the presence of rete ridges. HTSs resulting from burn wounds that healed without split thickness autografts were first investigated. The number of rete ridges was higher in normal skin compared to HTS that was either hypo- or hyperpigmented (1.31 ± 0.04 vs. 1.13 ± 0.05 and 1.14 ± 0.04 vs, p&lt; 0.05). This difference was similar despite pigmentation phenotype. When hyper-pigmented scars resulting from wounds that were treated with split thickness autografts (Hyper(+)) were investigated, rete ridge number was significantly higher than in Hyper(-) (1.89 ± 0.23, p&lt; 0.01). Patient age showed a weak correlation (R=-0.33) with rete ridge ratio where older patients had lower rete ridge ratios in normal, un-injured skin. Hyper(+) showed a weak correlation between rete ridge ratio and age of scar (R=-0.38). Conclusions Post-burn HTS that is dyschromic has fewer rete ridges than normal skin. This finding may explain the decreased epidermal barrier function that is associated with HTS.

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