ArticleBMC genomics2021
Inhibition of CUB and sushi multiple domains 1 (CSMD1) expression by miRNA-190a-3p enhances hypertrophic scar-derived fibroblast migration in vitro.
Article in BMC genomics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 55 citations in OpenAlex.
- Idiopathic Pulmonary Fibrosis: Analysis of Predisposing Variants in Patients with Familial Forms.Biomedicines · 2026Article
- Bazedoxifene Targets gp130 Signaling to Suppress Fibroblast Activation in Pathological Cutaneous Fibrosis: Insights from Spatial Transcriptomics and scRNA-seq Data.International journal of biological sciences · 2026Article
- Deciphering the cellular landscape of pathological scars.Burns & trauma · 2026Article
- Augmenting AMPA receptor signaling after spinal cord injury increases ependymal-derived neural stem/progenitor cell migration and promotes functional recovery.Nature neuroscience · 2025Article
- ALKBH3-Mediated MAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Identification of gene-sun exposure interactions of GWAS-identified variants in perceived facial aging progression.Frontiers in aging · 2025Article
- Targeting microRNA-190a halts the persistent myofibroblast activation and oxidative stress accumulation through upregulation of Krüppel-like factor 15 in oral submucous fibrosis.Journal of dental sciences · 2024Article
- Targeting the nuclear long noncoding transcript LSP1P5 abrogates extracellular matrix deposition by trans-upregulating CEBPA in keloids.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- HSFAS mediates fibroblast proliferation, migration, trans-differentiation and apoptosis in hypertrophic scars via interacting with ADAMTS8.Acta biochimica et biophysica Sinica · 2024Article
- ALKBH5-mediated mInflammation and regeneration · 2023Article
- [Research advances on the role and mechanism of microRNA in hypertrophic scar].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2023Article
- [Effects of mechanical tension on the formation of hypertrophic scars in rabbit ears and transforming growth factor-βZhonghua shao shang yu chuang mian xiu fu za zhi · 2022Article
- Exosome Derived from Mesenchymal Stem Cells Alleviates Pathological Scars by Inhibiting the Proliferation, Migration and Protein Expression of Fibroblasts via Delivering miR-138-5p to Target SIRT1.International journal of nanomedicine · 2022Article
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9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHypertrophic scar (HTS) is a fibroproliferative skin disorder characterized by excessive cell proliferation, migration, and extracellular matrix (ECM) deposition. The CUB and Sushi multiple domains 1 (CSMD1) has previously been identified as the key regulatory gene of hypertrophic scar by a large sample GWAS study. However, further research has not yet been conducted to verify this finding in other HTS patients and to determine the underlying mechanism.
resultsIn this study, we verified that CSMD1 was downregulated in both HTS tissue and HTS-derived fibroblasts. The knockdown of CSMD1 resulted in enhanced migration and fibronectin1 (FN1) secretion in fibroblasts in vitro. In addition, the upstream and downstream regulatory mechanisms of CSMD1 were also investigated through microRNA (miRNA) databases screening and RNA-sequencing (RNA-seq) respectively. The screening of four common microRNA (miRNA) databases suggested that miR-190a-3p binds to the CSMD1 and may regulate its expression. We confirmed that miR-190a-3p directly targeted the CSMD1-3'-UTR using luciferase reporter assays. Furthermore, the overexpression of miR-190a-3p showed promotion of migratory activity and FN1 secretion in fibroblasts, resembling the effect of CSMD1 knockdown; whereas the knockdown of miR-190a-3p exerted the opposite effect. Finally, transcriptomic analysis showed activation of Janus kinase-signal transducer and activator of transcription (JAK/STAT) signaling pathway in the CSMD1 knockdown fibroblasts.
conclusionsThis study has validated the conclusions of the previous GWAS study conducted in Chinese population. In vitro experiments have provided further evidence on the function of CSMD1 in the development of HTS, and have also revealed the underlying upstream and downstream regulating mechanisms. Additionally, the JAK/STAT signaling pathway identified using RNA-seq might provide a potential treatment approach, especially for HTS.
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