ArticleJournal of clinical medicine2022
The Expression of Follistatin-like 1 Protein Is Associated with the Activation of the EMT Program in Sjögren's Syndrome.
Article in Journal of clinical medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Signalling pathways regulated by FSTL1 in inflammation and potential therapeutic applications (Review).International journal of molecular medicine · 2026Review
- Immune and non-immune mediators in the fibrosis pathogenesis of salivary gland in Sjögren's syndrome.Frontiers in immunology · 2024Review
- Cellular Transcriptomics of Carboplatin Resistance in a Metastatic Canine Osteosarcoma Cell Line.Genes · 2023Article
- Molecular Mechanisms Linking Inflammation to Autoimmunity in Sjögren's Syndrome: Identification of New Targets.International journal of molecular sciences · 2022Review
- Special Issue "Diseases of the Salivary Glands-Part II".Journal of clinical medicine · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe activation of the epithelial to mesenchymal transition (EMT) program is a pathological response of the Sjögren's syndrome (SS) salivary glands epithelial cells (SGEC) to chronic inflammation. Follistatin-like 1 protein (FSTL1) is a secreted glycoprotein induced by transforming growth factor-β1 (TGF-β1), actively involved in the modulation of EMT. However, the role of FSTL1 in the EMT program activation in SS has not yet been investigated.
methodsTGF-β1-stimulated healthy human SGEC, SS SGEC, and SS salivary glands (SGs) biopsies were used to assess the effect of FSTL1 on the activation of the EMT program. FSTL1 gene activity was inhibited by the siRNA gene knockdown technique.
resultsHere we reported that FSTL1 is up-regulated in SS SGs tissue in a correlated manner with the inflammatory grade. Blockage of FSTL1 gene expression by siRNA negatively modulates the TGF-β1-induced EMT program in vitro. We discovered that these actions were mediated through the modulation of the SMAD2/3-dependent EMT signaling pathway.
conclusionsOur data suggest that the TGF-β1-FSTL1-SMAD2/3 regulatory circuit plays a key role in the regulation of EMT in SS and targeting FSTL1 may be a strategy for the treatment of SGs EMT-dependent fibrosis.
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