Effects of Intracordal Estradiol and Dexamethasone Injection on Wound Healing in Vocal Fold Injuries

Yıldız, Muhammet; Yiğit, Özgür; Sünter, Ahmet Volkan; Edızer, Deniz Tuna; Dursun, Nevra; Okçu, Oğuzhan

doi:10.1016/j.jvoice.2018.01.020

Cited by 9 publications

(11 citation statements)

References 34 publications

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“…These phenomena were consistent with previous work, 42 but warrant further investigation. Combined E2/TGF‐β1 treatment had no effect on Eln mRNA expression relative to TGF‐β1 alone, seemingly inconsistent with a previous report on rabbit vocal fold injuries 27 . Previous study reported that topically applied estrogen enhanced cutaneous wound repair, repressing neutrophil recruitment and resultant secretion of the degradative enzyme elastase 11 .…”

Section: Discussioncontrasting

confidence: 63%

Mechanisms Underlying the Antifibrotic Potential of Estradiol for Vocal Fold Fibrosis

et al. 2020

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Objectives/Hypothesis: Vocal fold fibrosis remains a significant clinical challenge. Estrogens, steroid hormones predominantly responsible for secondary sexual characteristics in women, have been shown to alter wound healing and limit fibrosis, but the effects on vocal fold fibrosis are unknown. We sought to elucidate the expression of estrogen receptors and the effects of estrogens on TGF-β1 signaling in rat vocal fold fibroblasts (VFFs).Study Design: In vitro. Methods: VFFs were isolated from 10-week-old, male Sprague-Dawley rats, and estrogen receptor alpha (ERα) and G protein-coupled receptor 30 (GPR30) were examined via immunostaining and quantitative polymerase chain reaction (qPCR). VFFs were treated with estradiol (E2, 10 −7 , 10 −8 or 10 −9 M) AE transforming growth factor beta 1 (TGF-β1, 10 ng/mL). ICI 182,780 (ICI, 10 −7 M) or G36 (10 −7 M) were employed as antagonists of ERα or GPR30, respectively. qPCR was employed to determine estrogen receptor-mediated effects of E2 on genes related to fibrosis.Results: ERα and GPR30 were expressed in VFFs at both the protein and the mRNA levels. E2 (10 −7 M) did not alter Smad3, Smad7, Acta2 mRNA, or extracellular matrix related genes. However, the combination of E2 (10 −8 M) and TGF-β1 significantly increased Smad7 (P = .03) and decreased Col1a1 (P = .04) compared to TGF-β1 alone; this response was negated by the combination of ICI and G36 (P = .009).Conclusions: E2 regulated TGF-β1/Smad signaling via estrogen receptors in VFFs. These findings provide insight into potential mechanisms of estrogens on vocal fold injury with the goal of enhanced therapeutics for vocal fold fibrosis.

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Section: Discussioncontrasting

confidence: 63%

Mechanisms Underlying the Antifibrotic Potential of Estradiol for Vocal Fold Fibrosis

et al. 2020

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“…Yıldız et al used estradiol and dexamethasone in the rat model with vocal cord injury. They did not find any significant differences when comparing the treated group with the group receiving saline [15]. In another study, basic fibroblast growth factor was shown to reduce vocal cord scar formation [16].…”

Section: Discussionmentioning

confidence: 94%

Effects of phenytoin injection on vocal cord healing after mechanical trauma: An experimental study

et al. 2019

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Background/aim: Phenytoin is an anticonvulsant drug which causes fibroblast proliferation, collagen synthesis, and an increase in epidermal growth factor. Therefore, the aim of the present study is to evaluate the effect of phenytoin injection on the wound healing process in rats with vocal cord injury by histopathological methods. Materials and methods: The vocal cords of 10 albino Wistar rats were damaged bilaterally; the left vocal cord was kept as the control group. Phenytoin was injected in the right vocal cord. Ten rats were sacrificed. The thickness of the lamina propria and density of the fibroblast and collagen were evaluated histopathologically. Results: Thickness of the lamina propria was 18.0 ± 7.1 µm in the control group, 65.5 ± 10.7 µm in the phenytoin group. The density of fibroblast and collagen were statistically lower in the control group compared the phenytoin group (P < 0.05). Conclusion: Phenytoin injection in rats after vocal cord injury significantly increased the thickness of the lamina propria and density of fibroblast and regular and mature collagen in the lamina propria. The findings in our study provide a feasible scientific view for adding phenytoin treatment to vocal cord surgeries in otolaryngology practice, but further studies are needed in order to evaluate the use of phenytoin in preventing the formation of scar tissue and possible effects on vocal cord vibration in humans after vocal cord injury.

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“…Furthermore, four out of the six PRL-promoters ( Figure 3 ) were found enriched in steroid hormone responding pathways, including SPP1, PRKCA, ADRB2, and LOX (see Table 2 and Supplementary Materials: Pathway_PRL_promoters). It has been suggested that injectable estradiol and dexamethasone might have similar effects on wound healing in VF injuries [ 23 ]. These results could help in understanding the association between VF injury and PRL and the possible roles that PRL plays in the VF wound healing.…”

Section: Discussionmentioning

confidence: 99%

Prolactin may serve as a regulator to promote vocal fold wound healing

Wang

et al. 2020

Bioscience Reports

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Reduced prolactin (PRL) has been shown to delay wound healing with a limited understanding of the underlying mechanisms. Here, we aim to explore the role of PRL in the repair of vocal fold (VF) injury. A microarray was used to detect the expressed levels of PRL in rat VF tissue at one, four, and eight weeks after VF injury compared with normal uninjured rats. Then a systematic bioinformatics analysis has been conducted to explore the literature-based biology network and signaling pathways involved in the repair of VF injury. The expression of PRL was significantly decreased in all VF injury groups (week one, week four, and week eight) compared to the control group (F stats=280.34; p=4.88e-14), with no significant difference among the three VF injury groups (F stats=1.97; p=0.18). Wounding has been shown to interfere with both PRL-promoting and inhibiting pathways that were involved in wound healing, including 11 PRL inhibitors and 6 PRL promoters. Our results reveal decreased PRL expression levels in VF injury, which is not in favor of the wound healing. The pathways identified may help in understanding the role of PRL as a treatment target for VF wound healing.

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Effects of Intracordal Estradiol and Dexamethasone Injection on Wound Healing in Vocal Fold Injuries

Cited by 9 publications

References 34 publications

Mechanisms Underlying the Antifibrotic Potential of Estradiol for Vocal Fold Fibrosis

Mechanisms Underlying the Antifibrotic Potential of Estradiol for Vocal Fold Fibrosis

Effects of phenytoin injection on vocal cord healing after mechanical trauma: An experimental study

Prolactin may serve as a regulator to promote vocal fold wound healing

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