Hyperbaric oxygen therapy can ameliorate the EMT phenomenon in keloid tissue

Abstract

Background:Hyperbaric oxygen therapy (HBOT) has been widely used in the clinical setting. In this study, HBOT therapy was evaluated for its ability to ameliorate the epithelial-to-mesenchymal transition (EMT) phenomenon in keloid tissue.Methods:Keloid patients were randomly divided into two groups: keloid patients (K group, 9 patients) and keloid patients receiving HBOT (O group, 9 patients). A third group with normal skin (S group, 9 patients) was established for control. Before HBOT and surgery, a laser Doppler flowmeter was used to measure the keloid blood supply of patients in the O group. Hematoxylin and eosin (H&E) staining was used to observe morphology. E-cadherin, ZO-1, vimentin, fibronectin, vascular endothelial growth factor (VEGF), and hypoxia inducible factor (HIF)-1α were measured by immunofluorescence staining and Western blot analysis. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to evaluate the mRNA expression level of these factors as well.Results:In the O group, keloid blood perfusion was significantly reduced after patients received HBOT. Compared with the K group, lower expression levels of vimentin, vibronectin, VEGF, and HIF-1α were observed in the O group, whereas the expression of E-cadherin and ZO-1 was significantly higher. The mRNA expression of E-cadherin and ZO-1 was also increased after HBOT.Conclusions:The expression levels of factors related to the EMT phenomenon were significantly reversed in keloid patients after they received HBOT, indicating that HBOT may be an effective therapy against the EMT phenomenon in keloid patients.

Hyperbaric oxygen treatment on keloid tumor immune gene expression

“…[ 12 ] The molecular biologic effects of HBOT on keloids were also studied. Zhang et al [ 11 ] found that HBOT can ameliorate the keloid EMT process by influencing hypoxia inducible factor-1α(HIF-1α) expression. In addition, HBOT can also influence the expression of inflammatory factors, such as IL-12p40, macrophage inflammatory protein-1β(MIP-1β), Platelet derived growth factor (PDGF-BB), and IL-1R.…”

lncRNA‐H19/miR‐29a axis affected the viability and apoptosis of keloid fibroblasts through acting upon COL1A1 signaling

“…GAPDH, glyceraldehyde 3-phosphate dehydrogenase; lncRNA, long-chain noncoding RNA; miR-29a, microRNA-29a miRNAs has been documented to express aberrantly during TGF-β-stimulated EMT, 35 which was a featured phenomenon of keloid onset. 36 For example, the miR-200 family and miR-205 modified EMT of breast cancer through prohibiting expression of ZEB, and enforced downregulation of miR-200 expression could bring down E-cadherin expression evidently. 37 Within this investigation, we found that miR-29a expression in fibroblasts declined after being sponged by H19 (Figure 4), just as in ccRCC.…”

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“…A oxigenoterapia hiperbárica -OHBé caracterizada por exposição a 100% de oxigênio ambiente, sendo muito usada em lesões de difícil cicatrização, algumas doenças do sistema nervoso central e diminuir a incidência de inflamações. Além disso, a terapia induz a redução da expressão de HIF1-alfa, interleucina1Beta e fator de necrose tumoral (TNF) (ZHANG et al, 2018). Diante disso, ZHANG et al ( 2018) desenvolveu uma pesquisa clínica com 27 pacientes portadores de queloide e não queloide, escolhidos aleatoriamente.…”

“…Geralmente atinge apenas a derma, exceto na síndrome de Lowe a qual acomete tecidos epiteliais da córnea (HOCHMAN et al, 2004;ZHANG et al, 2018).…”

“…De forma molecular, no tecido da queloide ocorre o fenômeno Brazilian Applied Science Review, Curitiba, v.5, n.2, p. 1148-1156 mar./abr. 2021 de transição epitelial para mesenquimal, uma vez que a hipóxia ou fator induzível a hipóxia alfa (HIF1-alfa) transforma os queratinócitos em fibroblastos, explicando a proliferação invasiva tecidual (ZHANG et al, 2018).…”