LncRNA PICSAR binds to miR-485-5p and activates TGF-β1/Smad to promote abnormal proliferation of hypertrophic scar fibroblasts (HSFs) and excessive deposition of extracellular matrix (ECM)

• Published in: Medical molecular morphology Vol. 54; no. 4; pp. 337 - 345
• Main Authors: Xu, Sijia, Dong, Wenxin, Shi, Yu
• Format: Journal Article
• Language: English
• Published: Singapore Springer Singapore 01.12.2021; Springer Nature B.V
• Subjects: Anatomy; Cell Proliferation; Cholecystokinin; Cicatrix, Hypertrophic - genetics; Cicatrix, Hypertrophic - pathology; Extracellular matrix; Extracellular Matrix - genetics; Fibroblasts; Fibroblasts - pathology; Humans; Immunofluorescence; Immunoprecipitation; Kinases; Medicine; Medicine & Public Health; MicroRNAs - genetics; Molecular Medicine; Original Paper; Pathology; RNA, Long Noncoding - genetics; Signal transduction; Smad protein; Smad Proteins; Transforming Growth Factor beta1 - genetics; Transforming growth factor-b1; TGF-β1; Hypertrophic scar fibroblasts; Smad; LncRNA PICSAR; ECM; miR-485-5p
• ISSN: 1860-1480; 1860-1499
• DOI: 10.1007/s00795-021-00296-4

The purpose of this study is to explore whether LncRNA PICSAR binds to miR-485-5p and thereby activates TGF-β1/Smad signaling pathway, influencing the abnormal proliferation of fibroblasts and excessive deposition of ECM in hypertrophic scar formation. PICSAR and miR-485-5p expressions were detected by qPCR. Cell proliferation was examined by CCK-8. Protein expressions were determined by western blot. Immunofluorescence detected the Ki-67 expression. Dual-luciferase followed by immunoprecipitation was performed to verify the interaction between PICSAR and miR-485-5p. Interference with PICSAR inhibited the abnormal proliferation of hypertrophic scar fibroblasts (HSFs) and the excessive deposition of ECM. It was also confirmed in our study that MiR-485-5p is a direct target of PICSAR in HSFs. Additionally, inhibition of miR-485-5p reversed the effect of PICSAR knockdown in HSFs. LncRNA PICSAR binds to miR-485-5p and thereby activates TGF-β1/Smad signaling pathway, promoting the abnormal proliferation of fibroblasts and excessive deposition of ECM in hypertrophic scar formation.