ArticleBioengineered2021
Silencing of long noncoding INHBA antisense RNA1 suppresses proliferation, migration, and extracellular matrix deposition in human hypertrophic scar fibroblasts via regulating microRNA-141-3p/myeloid cell leukemia 1 axis.
Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Mechanism of Platelet-Rich Plasma in Promoting Diabetic Wound Healing via the PI3K/AKT Signaling Pathway to Regulate Collagen Synthesis and Angiogenesis.Journal of diabetes research · 2026Article
- LINC01711 modulates proliferation, migration, and extracellular matrix deposition of hypertrophic scar fibroblasts by targeting miR-34a-5p.Archives of dermatological research · 2025Article
- SNHG1 functions as a ceRNA in hypertrophic scar fibroblast proliferation and apoptosis through miR-320b/CTNNB1 axis.Archives of dermatological research · 2023Article
- The Transcriptomics of the Human Vein Transformation After Arteriovenous Fistula Anastomosis Uncovers Layer-Specific Remodeling and Hallmarks of Maturation Failure.Kidney international reports · 2023Article
- Tumor Necrosis Factor-Mediators of inflammation · 2023Article
- Danshensu alleviates bleomycin-induced pulmonary fibrosis by inhibiting lung fibroblast-to-myofibroblast transition via the MEK/ERK signaling pathway.Bioengineered · 2021Article
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long noncoding RNAs (lncRNAs) play vital roles in the progression of hypertrophic scar (HS). We aimed to explore the effect of lncRNA INHBA Antisense RNA1 (INHBA-AS1) in the formation of HS and identify the potential mechanisms. INHBA-AS1 and microRNA (miR)-141-3p expression in human HS fibroblasts (hHSFs) was determined using RT-qPCR. LncBase online database predicted that miR-141-3p could be a putative target of INHBA-AS1, and the interaction of them was verified by luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Subsequently, following INHBA-AS1 silencing, cell proliferation and migration were evaluated using CCK-8, wound healing and Transwell assays. And rescue experiments were conducted to analyze the impact of INHBA-AS1 and miR-141-3p on HS formation. Immunofluorescence assay was employed to examine the expression of extracellular matrix (ECM)-related proteins. Then, StarBase database predicated that myeloid cell leukemia 1 (MCL1) was a potential target of miR-141-3p, which was verified with luciferase reporter- and RIP assays. Finally, cell function and ECM deposition were determined after MCL1-downregulation. INHBA-AS1 was significantly elevated while miR-141-3p was notably reduced in hHSFs. And it was confirmed that miR-141-3p was directly targeted by INHBA-AS1. Moreover, INHBA-AS1 silencing markedly attenuated the proliferation, migration and ECM accumulation of hHSFs, which were restored after miR-141-3p silencing. Additionally, MCL1 was confirmed as a direct target of miR-141-3p, and MCL1-knockdown remarkably alleviated the proliferation, migration and ECM accumulation of hHSFs. INHBA-AS1-knockdown suppresses the formation of HS by regulating miR-141-3p/MCL1 pathway, suggesting a promising therapeutic target for HS treatment.
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