scholarly journals Is leukotriene B4 one of the keloid marker? a fibroblast keloid study

2019 ◽  
Author(s):  
Yuli Kurniawati ◽  
Oki Suwarsa ◽  
A. Achadiyani ◽  
Sudigdo Adi
Keyword(s):  
Normal Skin ◽  
Leukotriene B4 ◽  
Normal Fibroblast ◽  
Fibroblast Proliferation ◽  
Elisa Method ◽  
Inflammatory Phase ◽  
Keloid Fibroblast ◽  
Normal Skin Fibroblast ◽  
Tgf Β1 ◽  
Chemical Mediators

Keloid pathogenesis occurs due to the duration of prolonged inflammatory phase and increased production of various growth factors such as TGF-β1 which may cause increasing fibroblast proliferation and collagen synthesis. Existence of one of the chemical mediators released during inflammation, leukotriene B4 (LTB4), in keloid pathogenesis specifically in the phases of inflammation and proliferation, is still unclear. The purpose of the study is to analyze the levels of LTB4 in keloid. Methods: Fibroblast culture that was done by explanting keloid and normal skin of a keloid patient. Measurement of LTB4 on keloid and normal fibroblast was done by Elisa method. This experiment was run in triplicate. Statistical test was conducted by t test for the unpaired data and Anova test. The experiment was done at cell culture laboratory of Medical Faculty of Padjadjaran University Bandung. Levels of LTB4 in keloid fibroblast was higher than that of normal skin fibroblast (mean 23143.27 vs 18191.85 pg/ml; p<0.05). Conclusion, increased LTB4 levels in keloid fibroblast showed the existence of LTB4 role in the prolonged inflammatory process in keloid pathogenesis.

scholarly journals The Comparison of the Levels of Leukotriene B4, TGF-β1, Collagen in Keloid Fibroblasts and Normal Skin Fibroblast

OALib ◽  
2016 ◽  
Vol 03 (07) ◽  
pp. 1-7
Author(s):  
Yuli Kurniawati ◽  
Oki Suwarsa ◽  
Achadiyani Agung ◽  
Sudigdo Adi
Keyword(s):  
Skin Fibroblast ◽  
Normal Skin ◽  
Leukotriene B4 ◽  
Normal Skin Fibroblast ◽  
Tgf Β1 ◽  
Keloid Fibroblasts

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>

Exosomale microRNA-21 Promotes Keloid Fibroblast Proliferation and Collagen Production by inhibiting Smad7

2021 ◽  
Author(s):  
Qijie Li ◽  
Lu Fang ◽  
Junjie Chen ◽  
Siqi Zhou ◽  
Kai Zhou ◽  
...  
Keyword(s):  
Normal Skin ◽  
Cell Types ◽  
Skin Fibroblasts ◽  
Fibroblast Proliferation ◽  
Collagen Production ◽  
Protein Levels ◽  
Keloid Fibroblast ◽  
Collagen Iii ◽  
Smad3 Protein ◽  
Keloid Fibroblasts

Abstract In keloid fibroblasts, microRNA-21 (miR-21) enhances activation of the TGF-β–Smad-signaling pathway by downregulating Smad7 expression, thereby promoting keloid fibroblast proliferation and collagen production. However, it is unclear whether miR-21 performs the above-mentioned functions through exosomal transport. Here, we extracted exosomes from the culture supernatants of keloid and normal skin fibroblasts, and observed that exosomes from both cell types secreted exosomes; however, keloid fibroblasts secreted significantly more exosomal miR-21 than normal skin fibroblasts (P &lt; 0.001). Interestingly, we also observed that exosomal miR-21 could enter target keloid fibroblasts. In addition, inhibiting exosomal miR-21 upregulated Smad7 protein expression and reduced Smad2 and Smad3 protein levels in target keloid fibroblasts. Furthermore, inhibiting exosomal miR-21 downregulated collagen I and collagen III expression in target keloid fibroblasts, increased the proportion of apoptotic cells, and reduced cell proliferation. Taken together, these results show that exosomal miR-21 promoted proliferation and collagen production in keloid fibroblasts by inhibiting Smad7. Thus, we identified regulatory roles for miR-21 in promoting keloid fibroblast proliferation and participating in keloid formation and development. These findings imply that miR-21 may serve as a novel target for controlling the development of keloids.

scholarly journals Extracorporeal shock waves enhance normal fibroblast proliferation in vitro and activate mRNA expression for TGF-β1 and for collagen types I and III

2009 ◽  
Vol 80 (5) ◽  
pp. 612-617 ◽  
Author(s):  
Laura Berta ◽  
Annamaria Fazzari ◽  
Anna Maria Ficco ◽  
Patrizia Maurici Enrica ◽  
Maria Graziella Catalano ◽  
...  
Keyword(s):  
Shock Waves ◽  
Mrna Expression ◽  
Normal Fibroblast ◽  
Fibroblast Proliferation ◽  
Collagen Types ◽  
Extracorporeal Shock Waves ◽  
Proliferation In Vitro ◽  
Tgf Β1

Apigenin Alleviates Renal Fibroblast Activation through AMPK and ERK Signaling Pathways In Vitro

2020 ◽  
Vol 21 (11) ◽  
pp. 1107-1118
Author(s):  
Ningning Li ◽  
Zhan Wang ◽  
Tao Sun ◽  
Yanfei Lei ◽  
Xianghua Liu ◽  
...  
Keyword(s):  
Renal Fibrosis ◽  
Transforming Growth Factor ◽  
Therapeutic Potential ◽  
Protective Role ◽  
Fibroblast Proliferation ◽  
Fibroblast Activation ◽  
And Function ◽  
Activated Fibroblasts ◽  
Tgf Β1

Objective: Renal fibrosis is a common pathway leading to the progression of chronic kidney disease. Activated fibroblasts contribute remarkably to the development of renal fibrosis. Although apigenin has been demonstrated to play a protective role from fibrotic diseases, its pharmacological effect on renal fibroblast activation remains largely unknown. Materials and Methods: Here, we examined the functional role of apigenin in the activation of renal fibroblasts response to transforming growth factor (TGF)-β1 and its potential mechanisms. Cultured renal fibroblasts (NRK-49F) were exposed to apigenin (1, 5, 10 and 20 μM), followed by the stimulation of TGF-β1 (2 ng/mL) for 24 h. The markers of fibroblast activation were determined. In order to confirm the anti-fibrosis effect of apigenin, the expression of fibrosis-associated genes in renal fibroblasts was assessed. As a consequence, apigenin alleviated fibroblast proliferation and fibroblastmyofibroblast differentiation induced by TGF-β1. Result: Notably, apigenin significantly inhibited the fibrosis-associated genes expression in renal fibroblasts. Moreover, apigenin treatment significantly increased the phosphorylation of AMP-activated protein kinase (AMPK). Apigenin treatment also obviously reduced TGF-β1 induced phosphorylation of ERK1/2 but not Smad2/3, p38 and JNK MAPK in renal fibroblasts. Conclusion: In a summary, these results indicate that apigenin inhibits renal fibroblast proliferation, differentiation and function by AMPK activation and reduced ERK1/2 phosphorylation, suggesting it could be an attractive therapeutic potential for the treatment of renal fibrosis.

scholarly journals Growth Differentiation Factor-9 Promotes Fibroblast Proliferation and Migration in Keloids through the Smad2/3 Pathway

2016 ◽  
Vol 40 (1-2) ◽  
pp. 207-218 ◽  
Author(s):  
Zhaohua Jiang ◽  
Qingxiong Yu ◽  
Lingling Xia ◽  
Yi Zhang ◽  
Xiuxia Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Wound Healing ◽  
Growth Factor ◽  
Fibroblast Proliferation ◽  
Differentiation Factor ◽  
Cox 2 ◽  
And Migration ◽  
Tgf Β1 ◽  
Keloid Fibroblasts ◽  
Proliferation And Migration

Background: Keloids are fibroproliferative scars that develop as a result of a dysregulated wound healing process; however, the molecular mechanisms of keloid pathogenesis remain unclear. Keloids are characterized by the ability to spread beyond the original boundary of the wound, and they represent a significant clinical challenge. Previous work from our group suggested that growth differentiation factor (GDF)-9 plays a role in the invasive behavior of keloids. Here, we examined the involvement of GDF-9 in keloid formation and spread and elucidated a potential underlying mechanism. Methods: The expression of GDF-9, cyclooxygenase (COX)-2, vascular epidermal growth factor (VEGF)-C, matrix metalloprotease (MMP)-2, MMP-9, transforming growth factor (TGF)-β1, and the related signaling pathway components in human keloid tissues or keloid fibroblasts (kFBs) was monitored by qRT-PCR and western blot. A series of overexpression and silencing experiments in normal and keloid fibroblasts were used to modify the expression of GDF-9. The effects of GDF-9 on kFB proliferation and migration were assessed using the CCK-8, cell cycle and scratch wound healing assays. Results: GDF-9 promotes fibroblast proliferation and migration. GDF-9 silencing in kFBs decreased cell proliferation, blocked cell cycle progression, downregulated the angiogenic markers COX-2 and VEGF-C, and downregulated MMP-2 and MMP-9 expression, whereas it had no effect on the levels of TGF-β1. GDF-9 silencing significantly inhibited Smad2 and Smad3 phosphorylation in kFBs. Conclusions: GDF-9 promotes the proliferation and migration of kFBs via a mechanism involving the Smad2/3 pathway.

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