ArticleThe ocular surface2022
Secreted Ly-6/uPAR-related protein-1 (SLURP1) is a pro-differentiation factor that stalls G1-S transition during corneal epithelial cell cycle progression.
Article in The ocular surface, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- In situ spatial transcriptomics reveals novel markers of the limbal stem cell niche and ocular surface epithelia.Stem cell reports · 2026Article
- Immune Niche Formation Reveals Mechanisms of Tumor Dormancy and Targeting Opportunities.Research square · 2026Article
- Immune Niche Formation in Engineered Mouse Models Reveals Mechanisms of Tumor Dormancy.bioRxiv : the preprint server for biology · 2025Article
- CDK4/6 inhibitor-associated vortex keratopathy: a case report.BMC ophthalmology · 2025Article
- The Secreted Ly6/uPAR-Related Protein-1 (SLURP1) Protects the Cornea From Oxidative Stress.Investigative ophthalmology & visual science · 2025Article
- Comparative Analysis of Corneal Wound Healing: Differential Molecular Responses in Tears Following PRK, FS-LASIK, and SMILE Procedures.Biomedicines · 2024Article
- Psoriasis: What Is New in Markers of Disease Severity?Medicina (Kaunas, Lithuania) · 2024Review
- The Secreted Ly6/uPAR-Related Protein 1 (Slurp1) Modulates Corneal Angiogenic Inflammation Via NF-κB Signaling.Investigative ophthalmology & visual science · 2024Article
- Unveiling the potential of SLURP1 protein as a biomarker for prostate cancer screening.Frontiers in oncology · 2024Article
- Molecular nature of ocular surface barrier function, diseases that affect it, and its relevance for ocular drug delivery.The ocular surface · 2023Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
purposePreviously we demonstrated that the secreted Ly-6/uPAR related protein-1 (SLURP1), abundantly expressed in the corneal epithelium (CE) and secreted into the tear fluid, serves as an anti-inflammatory and anti-angiogenic molecule. Here we describe the Slurp1-null (Slurp1X-/-) mouse corneal phenotype for the first time.
methodsWe compared the 10-week-old wild type (WT) and Slurp1X-/- mouse corneal (i) histology by hematoxylin-eosin and periodic acid-Schiff's reagent staining, (ii) cell proliferation by immunostaining for Ki67, (iii) cell adhesion molecules by immunostaining for desmosomal and tight junction proteins, (iv) barrier function by fluorescein staining and (v) wound-healing by epithelial debridement. Effect of SLURP1 on cell cycle was quantified in human corneal limbal epithelial (HCLE) cells engineered to express SLURP1 (HCLE-SLURP1).
resultsWT and Slurp1X-/- corneal histology was largely comparable, other than a few loosely attached superficial cells in Slurp1X-/- corneas. Compared with the WT, Slurp1X-/- corneas displayed (i) increase in Ki67+ cells, (ii) altered expression and/or localization of tight junction proteins Tjp1 and Pard3, and desmosomal Dsp, (iii) increased superficial fragility and (iv) slower CE wound healing. HCLE-SLURP1 cells displayed (i) decrease in Ki67+ cells, (ii) increased cell number doubling time, (iii) stalling in G1-S phase transition during cell cycle, and (iv) downregulation of cyclins CCNE and CCND1/D2, cyclin-dependent kinases CDK4 and CDK6, and upregulation of CDK inhibitor p15/CDKN2B.
conclusionsCollectively, these results elucidate that Slurp1X-/- CE cell homeostasis is altered and suggest that SLURP1 is a pro-differentiation factor that stalls G1-S transition during cell cycle progression by downregulating cyclins and upregulating p15/CDKN2B.
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