Human gingival fibroblast secretome accelerates wound healing through anti-inflammatory and pro-angiogenic mechanisms

Ahangar, Parinaz; Mills, Stuart J.; Smith, Louise E.; Gronthos, Stan; Cowin, Allison J.

doi:10.1038/s41536-020-00109-9

Cited by 42 publications

(41 citation statements)

References 31 publications

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“…Oral ulcers heal through the same phases as cutaneous wounds, but there are some differences, such as the wet external environment, the presence of saliva and various cell morphologies [ 24 ]. The environment of oral ulcers directs drug delivery to the application of muco-adhesive formulation [ 25 , 26 ].…”

Section: Introductionmentioning

confidence: 99%

HPLC/MSn Profiling and Healing Activity of a Muco-Adhesive Formula of Salvadora persica against Acetic Acid-Induced Oral Ulcer in Rats

et al. 2021

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Salvadora persica L. (S. persica, Siwak) is an ethnic plant that is widely used for improving oral hygiene. This study aimed to provide a phytochemical profiling of S. persica ethyl acetate fraction (SPEAF) and to evaluate the healing activity of a muco-adhesive formula of the fraction against acetic acid-induced oral ulcers in rats. HPLC-ESI-QTOF-MS-MS analysis of SPEAF resulted in the tentative identification of 56 metabolites containing fatty acids (23%), urea derivatives (10.5%) and sulphur compounds (10%), in addition to several amides, polyphenols and organic acids (6.5%, 5% and 2%, respectively). For the first time, 19 compounds were identified from S. persica. In vitro and in vivo experiments indicated that the extract is non-toxic. SPEAF exhibited superior healing activities compared to both the negative and positive control groups on days 7 and 14 of tongue ulcer induction. This was confirmed by histopathological examinations of haematoxylin and eosin-stained (H&E) and Masson’s trichrome-stained tongue sections. Moreover, SPEAF showed potent anti-inflammatory activities, as evidenced by the inhibited expression of interleukin-6 (IL-6) and tumour necrosis alpha (TNF-α). Moreover, SPEAF exhibited potent antioxidant activity, as it prevented malondialdehyde (MDA) accumulation, reduced glutathione (GSH) depletion and superoxide dismutase (SOD) exhaustion. SPEAF significantly enhanced hydroxyproline tongue content and upregulated collagen type I alpha 1 (Col1A1) mRNA expression. SPEAF also improved angiogenesis, as shown by the increased mRNA expression of the angiopoietin-1 (Ang-1). In conclusion, S. persica has a wide range of secondary metabolites and ameliorates acetic acid-induced tongue ulcers in rats. This can be attributed, at least partly, to its anti-inflammatory, antioxidant, procollagen and angiogenic activities. These findings provide support and validity for the use of S. persica as a traditional and conventional treatment for oral disorders.

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Section: Introductionmentioning

confidence: 99%

HPLC/MSn Profiling and Healing Activity of a Muco-Adhesive Formula of Salvadora persica against Acetic Acid-Induced Oral Ulcer in Rats

et al. 2021

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“…This study employed human gingival fibroblasts (HGFs) since these cells are responsible for constant adaptation, regeneration, and wound healing. [ 43 ] They effectively seal soft tissue ability and subsequently are critical in sustaining inflammation in periodontal diseases. [ 44 ] Consequently, the healthy bioactivity of HGFs with S. o .‐coated titanium could be of great importance in forming peri‐implant soft tissue seal.…”

Section: Discussionmentioning

confidence: 99%

Multilayered Adsorption of Commensal Microflora on Implant Surfaces: an Unconventional and Innovative Method to Prevent Bacterial Infections Associated with Biomaterials

Rahim

Döll

Stumpp

et al. 2021

Adv Materials Inter

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tious bacteria around dental implants may lead to the formation of biofilms, [3] which can cause mucosal inflammation, which is associated with peri-implant bone loss and peri-implantitis. [4] The ongoing tissue damage and bone resorption hinder the integration of the implant into tissue. Moreover, biofilms exhibit strong antibiotic resistance and are therefore impervious to therapy. [5] Biofilm formation is a stepwise process starting from the initial bacterial adhesion, followed by microcolony formation and finally maturation into extracellular encased mature biofilms. [6] Initial bacterial adhesion is the most critical step in biofilm formation and strategies targeting the inhibition of bacterial adhesion may be of therapeutic value. [7] Recent progress in understanding the nature and complexity of biofilms has led to the development of antibiofilm strategies. Since antibiotics remain the "gold standard" therapeutics, local antibiotic delivery systems have been applied to implant surfaces to prevent initial bacterial adhesion. [8] Even though most antibiotics resist bacterial attachment simply by killing the bacteria, they increase the chance that antimicrobial resistance may develop. [9] In addition, antibiotics may kill healthy microflora and their prolonged intake will result in systemic side effects in patients. [10] Moreover, metal ions as antimicrobial agents, such as cationic compounds, semi or fully synthetic peptides, or metallic nanoparticles (silver, copper, and zinc) have been coated on implant surfaces to prevent bacterial biofilms. [11] These metallic nanoparticles triggered toxic effects at the implantation site, as well as systemic effects in other organs. [12] In the context of antifouling coatings, polymeric coatings were applied on implant materials to resist bacterial adhesion and issues of severe biofilm formation. [13] One of the critical strategies involves applying poly(ethylene glycol) (PEG) to fabricate surfaces that resist bacterial adhesion against Escherichia coli, Staphylococcus epidermidis, Streptococcus sanguinis, and Lactobacillus salivarius. [14] However, the fabrication of polymer coating involves a complicated process and the mechanism of bacterial resistance is not universal against each bacterial species. This ineffectiveness of coating could be mainly due to the complexity of the mechanisms through which bacteria attach Biomaterials may be colonized with infectious biofilms and this frequently leads to progressive loss of tissue. Bacteria encased within biofilms resist antibiotics and the host immune system. With life-threatening complications and the antibiotic resistance crisis, novel therapeutic approaches are essentially required to treat biofilm infections. Commensal microflora-particularly streptococci-modulate the immune system's ability to protect from pathogens. In imitation of this natural phenomenon, the present study describes a novel method of applying the commensal, Streptococcus oralis, as a coating on implants to prevent infectious biofilms. Implants are...

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“…Periodontitis aggravated gingival tissue disorder and cellular function impairment 28 . The biological function of HGFs is an important indicator of physical condition of gingival tissues, and their migration is critical for gingival tissue restoration under in ammation microenvironment 29,30 . CCK-8 assay and wound healing experiments revealed that LINC01126 silencing had no obvious effect on cell viability of HGFs.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA 01126 activates IL-6/JAK2/STAT3 pathway via serving as a sponge of miR-655-3p in periodontitis

Tang¹,

Li²,

Yu³

et al. 2021

Preprint

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Background Periodontitis is a serious threat to oral quality of life and overall health. Although our previous studies confirmed that long intergenic non-coding RNA 01126 (LINC01126) is aberrantly expressed in periodontitis tissues, there are few reports on the pathogenesis of LINC01126 in periodontitis. Our study investigated the biological functions of LINC01126 in periodontitis and the potential mechanism. Results An inflammatory model of human gingival fibroblasts (HGFs) was successfully established. LINC01126 silencing can alleviate lipopolysaccharide (LPS) induced cell inflammation, reduce cell apoptosis, and promote cell migration. As a "sponge" for miR-655-3p, LINC01126 inhibits its binding to mRNA of IL-6, thereby promoting inflammation progression and JAK2/STAT3 pathway activation. qRT- PCR, WB, and IHC results of clinical tissue samples further confirmed that miR-655-3p expression was down-regulated and IL-6/JAK/STAT3 was abnormally activated in periodontitis tissues. Conclusions Our results indicate that LINC01126, as an endogenous competitive RNA (ceRNA) of miR-655-3p, can promote IL-6/JAK3/STAT3 pathway activation, thereby promoting periodontitis pathogenesis. And this is the first study of miR-655-3p in inflammatory periodontal diseases. Our study reveales a new pathogenesis of periodontitis, and provides a new strategy for preventing and treating periodontitis.

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Human gingival fibroblast secretome accelerates wound healing through anti-inflammatory and pro-angiogenic mechanisms

Cited by 42 publications

References 31 publications

HPLC/MSn Profiling and Healing Activity of a Muco-Adhesive Formula of Salvadora persica against Acetic Acid-Induced Oral Ulcer in Rats

HPLC/MSn Profiling and Healing Activity of a Muco-Adhesive Formula of Salvadora persica against Acetic Acid-Induced Oral Ulcer in Rats

Multilayered Adsorption of Commensal Microflora on Implant Surfaces: an Unconventional and Innovative Method to Prevent Bacterial Infections Associated with Biomaterials

Long non-coding RNA 01126 activates IL-6/JAK2/STAT3 pathway via serving as a sponge of miR-655-3p in periodontitis

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