A key role of microRNA-26a in the scar formation after glaucoma filtration surgery

Wang, Weihong; Deng, Aijun; He, Sheng-guang

doi:10.1080/21691401.2017.1345926

Cited by 13 publications

(7 citation statements)

References 28 publications

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“…Abnormal expression of miRNAs may contribute to the management of skin fibrotic diseases ( 25 ). A recent study investigated the role of miR-26a in scar formation following glaucoma filtration surgery and the findings suggested that miR-26a served an essential role in filtering tract scar formation ( 26 ); however, these results were limited to the role of miR-26a in postoperative scar formation. The present study was conducted to investigate the role of miR-26a in HS.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-26a inhibits hyperplastic scar formation by targeting Smad2

Liu

et al. 2018

Exp Ther Med

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Hypertrophic scar (HS) is a fibrotic disease in which excessive extracellular matrix forms due to the response of fibroblasts to tissue damage. Novel evidence suggests that microRNAs (miRNAs or miRs) may contribute to hypertrophic scarring; however, the role of miRNAs in HS formation remains unclear. In the present study, miR-26a was significantly downregulated in HS tissues and human HS fibroblasts (hHSFs) was detected by reverse transcription-quantitative analysis. TargetScan was used to predict that mothers against decapentaplegic homolog 2 (Smad2) is a potential target gene of miR-26a and a dual-luciferase reporter assay confirmed that Smad2 was a target gene of miR-26a. The expression of Smad2 was upregulated in HS tissues and hHSFs. Cell Counting Kit-8 and flow cytometry analyses demonstrated that the overexpression of miR-26a significantly suppressed the proliferation ability of hHSFs and the apoptotic rate of hHSFs was significantly upregulated in response to miR-26a mimic transfection. Furthermore, the expression of B-cell lymphoma-2 (Bcl-2)-associated X protein was increased and Bcl-2 expression was decreased following miR-26a mimic transfection. The expression of collagens I and III was significantly inhibited following treatment with miR-26a mimics in hHSF cells. Conversely, miR-26a inhibitors served an opposing role in hHSFs. Furthermore, Smad2 overexpression enhanced the expression of collagens I and c III; however, Smad2 silencing inhibited the expression of collagens I and c III. In conclusion, the results of the present study indicate that miR-26a inhibits HS formation by modulating proliferation and apoptosis ad well as inhibiting the expression of extracellular matrix-associated proteins by targeting Smad2.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-26a inhibits hyperplastic scar formation by targeting Smad2

Liu

et al. 2018

Exp Ther Med

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“…Increasing evidence implicates mircoRNAs (miRNAs) as important regulatory factors in tumorigenesis and hypertrophic scars, and they are found to be dysregulated in the majority of analyzed cancers and pathological scars [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

miR-137 Inhibits Proliferation and Metastasis of Hypertrophic Scar Fibroblasts via Targeting Pleiotrophin

Zhang

Guo

Qiang

et al. 2018

Cell Physiol Biochem

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Background/Aims: There are few effective treatment options for hypertrophic scars. MircoRNAs are a class of small, noncoding RNAs involved in multiple biological functions. Methods: Gene chip screening was used to screen out the differential expression of miRNAs in hypertrophic scars and normal tissues. Western blot and real-time PCR were used to confirm the expression of pleiotrophin (PTN) in hypertrophic scars. After analyze the correlation between PTN and miR-137 using correlation analysis, we used miRDB software to analyze the binding sites of miR-137 and PTN. Luciferase reporter gene, western blot and real-time PCR experiments were used to detect the regulatory effect of miR-137 on PTN. MTT and transwell assay were used to detect the effect of miR-137 on proliferation and metastasis. Western blot and real-time PCR were used to detect the regulatory effects of miR-137 on cyclin B1, matrix metalloproteinase 9 (MMP9), α-smooth muscle actin (α-SMA), vimentin, and type-I collagen (COL1A). Finally, miR-137 inhibitor was transfected into fibroblasts which was silent PTN, and the proliferation and migration of cells were detected by MTT and transwell. Western blot and real-time PCR were used to detect the expression of related proteins. Results: Various miRNAs was abnormal expressed in hypertrophic scars. miR-137 was decreased in hypertrophic scar, however PTN was up regulated in hypertrophic scars. miR-137 induced proliferation and metastasis in fibroblasts. This effect was accompanied by decreased expression of cyclin B1, MMP9, α-SMA, vimentin, and COL1A mediated via the target of PTN. Conclusion: Modulation of miR-137 expression in fibroblasts could provide an important therapeutic strategy for hypertrophic scars.

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“…A recent study showed that expression of microRNA-26a was significantly down regulated in the HSs after glaucoma filtration surgery. 17 Overexpression of microRNA-26a has been proved to reduce the expression of collagen fibers in keloid and to restrain the occurrence of skin fibrosis. 18 In this study, the expression of microRNA-26a in HSs was significantly up- regulated after the treatment via triamcinolone acetonide, suggesting that microRNA-26a might be involved in the development of HS and its pathological process.…”

Section: Discussionmentioning

confidence: 99%

Treatment of hypertrophic scar with injection of triamcinolone leads to increased microRNA-26a in a rabbit ear model

2022

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Objectives: Differential expression of microRNAs (miRNAs) has been confirmed to promote hypertrophic scar (HS) formation. However, this mechanism remains to be further elucidated. This paper investigated the effects of microRNA26a on HS of rabbit ears or its mechanism. Methods: The rabbit HS models were established and randomly assigned to either the experimental group (20 rabbits with treatment through triamcinolone acetonide) or the scar group (20 rabbits without treatment). In addition, 10 unmodeled rabbits were served as control group. The expression of microRNA-26a in HS tissues was detected via a stem-loop real-time polymerase chain reaction (RT-PCR). Results: According to RT-PCR, we showed the decreased expression of microRNA-26a in the scar group compared with that in the experimental group, and in the experimental group compared with that in the control group ( p < .01). In addition, the expression of microRNA-26a was negatively correlated with scar thickness (STs), number of fibroblasts (NFs), Collagen I (Col I) level, Collagen III (Col III) level, Interleukin-6 (IL-6) level, and Tumor necrosis factor-alpha (TNF-α) level (all p < .01). Conclusions: Our findings revealed that the increase of microRNA-26a expression might alleviate excessive inflammation during the HS formation, inhibit fibroblast proliferation and collagen deposition in HS, and promote the treatment of HS.

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A key role of microRNA-26a in the scar formation after glaucoma filtration surgery

Cited by 13 publications

References 28 publications

MicroRNA-26a inhibits hyperplastic scar formation by targeting Smad2

MicroRNA-26a inhibits hyperplastic scar formation by targeting Smad2

miR-137 Inhibits Proliferation and Metastasis of Hypertrophic Scar Fibroblasts via Targeting Pleiotrophin

Treatment of hypertrophic scar with injection of triamcinolone leads to increased microRNA-26a in a rabbit ear model

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