Mediatory role of interleukin‐6 in α smooth muscle actin induction and myofibroblast formation around silicone tissue expander

Joseph, Josna; Variathu, Kumary Thrikkovil; Mohanty, Mira

doi:10.1002/jbm.a.34596

Cited by 8 publications

(5 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Apart from TGF-β, it has been shown that other pro-inflammatory cytokines also play critical roles in the persistent activation of myofibroblasts. Earlier studies have demonstrated the pro-fibrotic role of interleukin (IL)-6 in α-SMA induction [ 11 ] and the transition of fibroblasts into myofibroblast phenotypes [ 12 ]. Recently, it has been revealed that IL-6 could augment TGF-β/Smad signaling [ 13 ] and participate in the TGF-β1-mediated transdifferentiation of myofibroblasts [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

Positive Feedback Loop of SNAIL-IL-6 Mediates Myofibroblastic Differentiation Activity in Precancerous Oral Submucous Fibrosis

Peng

Liao

et al. 2020

Cancers

View full text Add to dashboard Cite

Oral submucosal fibrosis (OSF) is a premalignant disorder of the oral cavity, and areca nut chewing is known to be a major etiological factor that could induce epithelial to mesenchymal transition (EMT) and activate buccal mucosal fibroblasts (BMFs). However, this detailed mechanism is not fully understood. In this study, we showed that the upregulation of Snail in OSF samples and fibrotic BMFs (fBMFs) may result from constant irritation by arecoline, a major alkaloid of the areca nut. The elevation of Snail triggered myofibroblast transdifferentiation and was crucial to the persistent activation of fBMFs. Meanwhile, Snail increased the expression of numerous fibrosis factors (e.g., α-SMA and collagen I) as well as IL-6. Results from bioinformatics software and a luciferase-based reporter assay revealed that IL-6 was a direct target of Snail. Moreover, IL-6 in BMFs was found to further increase the expression of Snail and mediate Snail-induced myofibroblast activation. These findings suggested that there was a positive loop between Snail and IL-6 to regulate the areca nut-associated myofibroblast transdifferentiation, which implied that the blockage of Snail may serve as a favorable therapeutic strategy for OSF treatment.

show abstract

Section: Introductionmentioning

confidence: 99%

Positive Feedback Loop of SNAIL-IL-6 Mediates Myofibroblastic Differentiation Activity in Precancerous Oral Submucous Fibrosis

Peng

Liao

et al. 2020

Cancers

View full text Add to dashboard Cite

show abstract

“…This is accompanied by differentiation of fibroblasts into myofibroblasts mediated by the profibrotic cytokine TGF-β [ 52 ]. IL-6, has an additional profibrotic role in activating fibroblast to myofibroblast transition [ 53 ].…”

Section: Resultsmentioning

confidence: 99%

Effects of Silicone Breast Implants on Human Cell Types In Vitro: A Closer Look on Host and Implant

2022

View full text Add to dashboard Cite

Background Silicone (gel) breast implants (SBI) are used world-wide for breast augmentation, and reconstruction or to correct breast deformities. They consist of two compounds: an elastomer silicone shell (envelope) and a silicone gel filler (core). Breast Implant Illness (BII) is a term used for women with SBI, who suffer from various of symptoms including myalgia, arthralgia, fatigue, fever, dry eyes and/or dry mouth (sicca), as well as cognitive disturbances, which are rated by these woman as response to SBI. The pathogenesis of these adverse effects as well as the histocompatibility and the SBI-cell interaction of silicone and its surrounding tissue (implant-host tissue interface) is a subject of current research. The main purpose of this review is to provide an overview of the current knowledge regarding the effects of silicone (gel and elastomer surfaces) of a SBI on different human cell types from experimental - in vitro - models. Methods A comprehensive research was conducted by two independent reviewers in March and July of 2020 in the PubMed, MEDLINE, and Cochrane databases. Results A number of 1328 articles on this topic were initially identified, of which 62 could be finally included an analysed in this review. Conclusion SBI may lead to a physiologic pro-inflammatory and foreign body host response with fibrous encapsulation accompanied by a disturbed Th17/Treg balance and IL-17 production. No causal relationship is known for systemic symptoms and/or autoimmune outcomes in the context of BII. Level of Evidence III This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266.

show abstract

“…RAW 264.7 murine macrophages (1×10 4 cells/well) were maintained in 6-well plates containing each of the aforementioned materials for 24 h at 37 °C. Proinflammatory cytokines, interleukin (IL) 1β, IL6, tumor necrosis factor α (TNFα) and transforming growth factor β (TGFβ), have been reported to have critical roles in fibrosis generation after breast implant surgery (4,27). Therefore, the levels of these cytokines were assessed.…”

Section: Resultsmentioning

confidence: 99%

Roxatidine inhibits fibrosis by inhibiting NF‑κB and MAPK signaling in macrophages sensing breast implant surface materials

Wang

Tian

et al. 2019

Mol Med Report

View full text Add to dashboard Cite

Capsular contracture is an important complication after silicone mammary implant surgery. Fibroblasts and macrophages play critical roles in the pathogenesis of capsular contracture, making these two cell types therapeutic targets. It has been reported that inhibiting histamine receptors results attenuates fibrosis, but the role of roxatidine (a histamine receptor 2 inhibitor) in preventing fibrosis caused by breast implant materials remains unknown. The aim of the present study was to assess the hypothesis that roxatidine might have a prophylactic effect in capsular contracture induced by implant material. Inflammation induced by breast implant materials was mimicked by co-culturing macrophages or fibroblasts with these materials in vitro. Capsular contracture was modeled in mice by planting breast implant materials in a subcutaneous pocket. Roxatidine was added in the culture medium or administered to mice bearing breast implant materials. By co-culturing macrophages or fibroblasts with common breast implant materials (micro-textured or smooth breast implants), the present study demonstrated that macrophages respond to these materials by producing pro-inflammatory cytokines, a process that was abolished by addition of roxatidine to the culture medium. Although fibroblasts did not respond to implant surface materials in the same way as macrophages, the conditioned media of macrophages induced proliferation of fibroblasts. Mechanistically, administration of roxatidine inhibited activation of NF-κB and p38/mitogen-activated protein kinase (MAPK) signaling in macrophages. Furthermore, treatment with roxatidine in implant-bearing mice reduced serum concentrations of transforming growth factor-β and the abundance of fibroblasts around the implant. The present study concluded that roxatidine plays an important role in preventing fibrosis by inhibiting activation of NF-κB and p38/MAPK signaling in macrophages.

show abstract

Mediatory role of interleukin‐6 in α smooth muscle actin induction and myofibroblast formation around silicone tissue expander

Cited by 8 publications

References 21 publications

Positive Feedback Loop of SNAIL-IL-6 Mediates Myofibroblastic Differentiation Activity in Precancerous Oral Submucous Fibrosis

Positive Feedback Loop of SNAIL-IL-6 Mediates Myofibroblastic Differentiation Activity in Precancerous Oral Submucous Fibrosis

Effects of Silicone Breast Implants on Human Cell Types In Vitro: A Closer Look on Host and Implant

Roxatidine inhibits fibrosis by inhibiting NF‑κB and MAPK signaling in macrophages sensing breast implant surface materials

Contact Info

Product

Resources

About