Functional Study Of SNHG26 In Promoting Keloid Fibroblast Proliferation, Extracellular Matrix Synthesis And Inflammatory Respons

BackgroundKeloid is an excessive tissue response to dermal injury,which can affect the physical and mental health of patients to varying degrees.Long non-coding RNAs(lncRNAs)are a type of non-coding RNA with a length of more than 200 nucleotides.Compared with protein-coding genes,lncRNAs have more tissue-and cell-specific expression and functions,and therefore have more potential in the diagnosis and treatment of diseases.Increasing evidence suggests that the expression levels of various lncRNAs change in keloids and can participate in keloid formation and development through various pathways.ObjectiveTo investigate the expression of SNHG26 in keloid tissue and its impact on the function of normal and keloid-derived fibroblasts.MethodsFirst,RT-qPCR was used to detect the expression of SNHG26 in keloid and surrounding normal skin tissue.Then,MACS magnetic bead separation was used to isolate different types of cells in the tissue,and RT-qPCR was used to detect the expression of SNHG26 in various types of cells.Finally,RNA-scope technology was used to detect the localization and quantification of SNHG26 in keloid tissue and fibroblasts.In terms of functional experiments,clone formation assays were used to detect the effect of knockdown of SNHG26 in fibroblasts on the proliferation of normal skin fibroblast and keloid fibroblast.RT-qPCR was used to detect the effect of SNHG26 knockdown on the extracellular matrix synthesis and TNFα-induced inflammatory response of NF and KF.Finally,RT-qPCR was used to detect the upstream cytokines of SNHG26 in fibroblasts.ResultsSNHG26 expression was upregulated in keloid tissue and keloid fibroblasts;Knockdown of SNHG26 in fibroblasts inhibited NF and KF proliferation,extracellular matrix synthesis and inflammatory factor secretion;TNFα significantly induced SNHG26 expression in skin fibroblasts.ConclusionOur study first discovered that SNHG26 was upregulated in keloid tissue and fibroblasts and that its knockdown could inhibit the proliferation of NF and KF,extracellular matrix synthesis,and inflammatory cytokine secretion.Furthermore,TNFαcan induce the expression of SNHG26 in fibroblasts.These results suggest that SNHG26 may be a key pathogenic molecule in keloid formation and could become a new target for the treatment of keloid disease.