June 2022
Volume 63, Issue 7
Open Access
ARVO Annual Meeting Abstract  |   June 2022
Secreted Ly-6/uPAR Related Protein-1 (SLURP1) Suppresses Canonical TGF-b Signaling in Corneal Epithelial Cells
Author Affiliations & Notes
  • Sudha Swamynathan
    Ophthalmology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States
  • Shivalingappa K Swamynathan
    Ophthalmology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States
  • Footnotes
    Commercial Relationships   Sudha Swamynathan University of Pittsburgh, patent number-9731014, Code P (Patent); Shivalingappa Swamynathan University of Pittsburgh, patent number-9731014, Code P (Patent)
  • Footnotes
    Support  RO1 EY022898, RO1 EY031684, P30 EY08098, Unrestricted grants from RPB and Eye and Ear Foundation of Pittsburgh
Investigative Ophthalmology & Visual Science June 2022, Vol.63, 3258 – A0293. doi:
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      Sudha Swamynathan, Shivalingappa K Swamynathan; Secreted Ly-6/uPAR Related Protein-1 (SLURP1) Suppresses Canonical TGF-b Signaling in Corneal Epithelial Cells. Invest. Ophthalmol. Vis. Sci. 2022;63(7):3258 – A0293.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : Secreted Ly-6/uPAR Related Protein-1 (SLURP1), abundantly expressed by the corneal epithelium (CE) and secreted to the tear film, is an anti-inflammatory protein with anti-tumor properties. TGF-b pathway has diverse roles in tissue homeostasis as well as pathological conditions including epithelial-mesenchymal transition (EMT) during tumor metastasis. Here, we studied the influence of SLURP1 on canonical TGF-b signaling using Slurp1X-/- mouse cornea and human corneal limbal epithelial (HCLE) cells.

Methods : The effect of Slurp1 ablation on TGF-b signaling was studied by comparing TGF-b Receptor 2 (TGFBR2), Smad4, and phospho-Smad2/3 expression in wild type (WT) and Slurp1X-/- mouse corneas by immunoblots and immunofluorescent staining. The effect SLURP1 on TGF-b signaling was analyzed by comparing the TGF-b-induced Smad2/3 phosphorylation and E-cadherin expression in HCLE and HCLE-SLURP1 cells engineered to over-express SLURP1.

Results : Slurp1X-/- mouse corneas displayed elevated expression (127% of WT) and prominent nuclear localization of TGFBR2, coupled with elevated expression of Smad4, and phospho-Smad2/3. Upon stimulation with 5ng/ml TGF-b, HCLE-SLURP1 displayed decreased SMAD2/3 phosphorylation compared with that in HCLE cells. After 1h of TGF-b addition, the phospho-SMAD2/Total SMAD2 ratio was 20% lower in HCLE-SLURP1 compared with HCLE cells. Upon TGF-b treatment, E-cadherin expression decreased to a greater extent in HCLE compared with HCLE-SLURP1 cells. Confluent HCLE-SLURP1 cells retained E-cadherin in their cell membranes more efficiently than HCLE cells at 24h and 48h after TGF-b addition.

Conclusions : Increased expression of TGFBR2, Smad4 and pSmad2/3 indicate higher canonical TGF-b signaling activity in Slurp1X-/- corneas. SLURP1 suppresses canonical TGF-b signaling in HCLE cells and protects E-cadherin from TGF-b induced disintegration, consistent with a role for SLURP1 in protecting the CE cells from TGF-b-induced EMT.

This abstract was presented at the 2022 ARVO Annual Meeting, held in Denver, CO, May 1-4, 2022, and virtually.

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