Abstract
Purpose: To systematically analyze the overall m6A modification pattern in hyperplastic scars (HS).Methods: The m6A modification patterns in HS and normal skin (NS) tissues were described by m6A sequencing and RNA sequencing, and subsequently bioinformatics analysis was performed. The m6A-related RNA was immunoprecipitated and verified by real-time quantitative PCR.Results: The appearance of 14,791 new m6A peaks in the HS sample was accompanied by the disappearance of 7,835 peaks. The unique m6A-related genes in HS were thus associated with fibrosis-related pathways. We identified the differentially expressed mRNA transcripts in HS samples with hyper-methylated or hypo-methylated m6A peaks.Conclusion: This study is the first to map the m6A transcriptome of human HS, which may help clarify the possible mechanism of m6A-mediated gene expression regulation.
Highlights
Hypertrophic scars (HS) normally occur after burns and trauma
This study is the first to map the m6A transcriptome of human HS, which may help clarify the possible mechanism of m6A-mediated gene expression regulation
Specialty section: This article was submitted to Developmental Epigenetics, a section of the journal Frontiers in Cell and Developmental
Summary
Hypertrophic scars (HS) normally occur after burns and trauma. The pathological features of hypertrophic scars include abnormal inflammation, excessive proliferation and differentiation of fibroblasts, increased angiogenesis, and excessive deposition of extracellular matrix (ECM) (Zhu et al, 2020; Zhang et al, 2021). It is difficult to achieve a complete cure by traditional surgery, radiotherapy, and hormone therapy, in areas where HS are prone to recurrence (Jaloux et al, 2017). Scar repair has always been a difficult and hot spot in the field of wound repair and plastic surgery. Studies have shown that regulatory factors including epigenetic DNA methyltransferase, non-coding RNA, and histones are dysregulated in skin fibrosis m6A and Hypertrophic Scar (Mann and Mann, 2013; Hardy and Mann, 2016; Lee et al, 2017)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
