Use of Mitomycin-C in Laryngotracheal Stenosis

Felice, Christopher Di; Machuzak, Michael; Shepherd, Ray W.

doi:10.1097/lbr.0000000000000933

Cited by 3 publications

(1 citation statement)

References 36 publications

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“…Evidence suggests that MMC is a safe and effective option in the endoscopic therapy of laryngotracheal stenosis. 17 In 2023, however, Felice et al 18 reviewed and synthesized the existing literature on MMC as an adjunctive therapy for laryngotracheal stenosis. Finally, they found that the role of MMC as an adjunctive therapy in LTS is not certain.…”

Section: Discussionmentioning

confidence: 99%

Down‐regulation of miR‐21‐5p by pirfenidone to inhibit fibroblast proliferation in the treatment of acquired tracheal stenosis

Li,

Huang,

Wei

et al. 2023

Clinical Respiratory J

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ObjectiveTreatment options for acquired tracheal stenosis (ATS) are limited due to a series of pathophysiological changes including inflammation and cell proliferation. Micro ribonucleic acid‐21‐5p (miR‐21‐5p) may promote the excessive proliferation of fibroblasts. However, various types of fibrosis can be prevented with pirfenidone (PFD). Currently, the effect of PFD on miR‐21‐5p and its biological function has not been clarified. In this study, PFD was evaluated as a potential treatment for ATS by inducing fibroblast proliferation in lipopolysaccharide (LPS)‐induced fibroblasts by targeting miR‐21‐5p.MethodsFor 48 h, 1 g/ml LPS was used to generate fibroblasts in vitro, followed by the separation of cells into four groups: control, PFD, mimic, and mimic + PFD. The Cell Counting Kit‐8 (CCK‐8) technique was adopted to measure the proliferation of fibroblasts. Real‐time quantitative polymerase chain reaction (RT‐qPCR) and Western blot (WB) were used to measure the relative expressions of tumor necrosis factor‐α (TNF‐α), transforming growth factor‐β1 (TGF‐β1), drosophila mothers against decapentaplegic 7 (Smad7) and collagen type I alpha 1(COL1A1) messenger RNA (mRNA) and proteins, respectively.Results(1) At 0, 24, 48, and 72 h, fibroblast growth was assessed using the CCK‐8 method. Compared with the control group, the mimic group showed the highest fibroblast viability, and the PFD group showed the lowest fibroblast viability. However, fibroblast viability increased in the mimic + PFD group but decreased in the mimic one. (2) RT‐qPCR and WB showed that the mimic group exhibited a significant up‐regulation in the relative expressions of TNF‐α, TGF‐β1, and COL1A1 mRNA and proteins but a down‐regulation in the relative expression of Smad7 mRNA and protein compared with the control one. In the PFD group, the results were the opposite. Nevertheless, the relative expressions of TNF‐α, TGF‐β1, and COL1A1 mRNA and proteins were increased, whereas that of Smad7 mRNA was decreased in the mimic + PFD group. The change was less in the mimic group.ConclusionPFD may have a preventive and curative effect on ATS by inhibiting fibroblast proliferation and the fibrotic process and possibly through down‐regulating miR‐21‐5p and up‐regulating Smad7 and its mediated fibrotic and inflammatory responses.

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Section: Discussionmentioning

confidence: 99%