The SULFs, Extracellular Sulfatases for Heparan Sulfate, Promote the Migration of Corneal Epithelial Cells during Wound Repair

Maltseva I, Chan M, Kalus I, Dierks T, Rosen SD (2013)
PloS one 8(8): e69642.

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Zeitschriftenaufsatz | Veröffentlicht | Englisch
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Abstract / Bemerkung
Corneal epithelial wound repair involves the migration of epithelial cells to cover the defect followed by the proliferation of the cells to restore thickness. Heparan sulfate proteoglycans (HSPGs) are ubiquitous extracellular molecules that bind to a plethora of growth factors, cytokines, and morphogens and thereby regulate their signaling functions. Ligand binding by HS chains depends on the pattern of four sulfation modifications, one of which is 6-O-sulfation of glucosamine (6OS). SULF1 and SULF2 are highly homologous, extracellular endosulfatases, which post-synthetically edit the sulfation status of HS by removing 6OS from intact chains. The SULFs thereby modulate multiple signaling pathways including the augmentation of Wnt/ß-catenin signaling. We found that wounding of mouse corneal epithelium stimulated SULF1 expression in superficial epithelial cells proximal to the wound edge. Sulf1(-/-) , but not Sulf2(-/-) , mice, exhibited a marked delay in healing. Furthermore, corneal epithelial cells derived from Sulf1(-/-) mice exhibited a reduced rate of migration in repair of a scratched monolayer compared to wild-type cells. In contrast, human primary corneal epithelial cells expressed SULF2, as did a human corneal epithelial cell line (THCE). Knockdown of SULF2 in THCE cells also slowed migration, which was restored by overexpression of either mouse SULF2 or human SULF1. The interchangeability of the two SULFs establishes their capacity for functional redundancy. Knockdown of SULF2 decreased Wnt/ß-catenin signaling in THCE cells. Extracellular antagonists of Wnt signaling reduced migration of THCE cells. However in SULF2- knockdown cells, these antagonists exerted no further effects on migration, consistent with the SULF functioning as an upstream regulator of Wnt signaling. Further understanding of the mechanistic action of the SULFs in promoting corneal repair may lead to new therapeutic approaches for the treatment of corneal injuries.
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PloS one
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8
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8
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e69642
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Maltseva I, Chan M, Kalus I, Dierks T, Rosen SD. The SULFs, Extracellular Sulfatases for Heparan Sulfate, Promote the Migration of Corneal Epithelial Cells during Wound Repair. PloS one. 2013;8(8):e69642.
Maltseva, I., Chan, M., Kalus, I., Dierks, T., & Rosen, S. D. (2013). The SULFs, Extracellular Sulfatases for Heparan Sulfate, Promote the Migration of Corneal Epithelial Cells during Wound Repair. PloS one, 8(8), e69642. doi:10.1371/journal.pone.0069642
Maltseva, I., Chan, M., Kalus, I., Dierks, T., and Rosen, S. D. (2013). The SULFs, Extracellular Sulfatases for Heparan Sulfate, Promote the Migration of Corneal Epithelial Cells during Wound Repair. PloS one 8, e69642.
Maltseva, I., et al., 2013. The SULFs, Extracellular Sulfatases for Heparan Sulfate, Promote the Migration of Corneal Epithelial Cells during Wound Repair. PloS one, 8(8), p e69642.
I. Maltseva, et al., “The SULFs, Extracellular Sulfatases for Heparan Sulfate, Promote the Migration of Corneal Epithelial Cells during Wound Repair”, PloS one, vol. 8, 2013, pp. e69642.
Maltseva, I., Chan, M., Kalus, I., Dierks, T., Rosen, S.D.: The SULFs, Extracellular Sulfatases for Heparan Sulfate, Promote the Migration of Corneal Epithelial Cells during Wound Repair. PloS one. 8, e69642 (2013).
Maltseva, Inna, Chan, Matilda, Kalus, Ina, Dierks, Thomas, and Rosen, Steven D. “The SULFs, Extracellular Sulfatases for Heparan Sulfate, Promote the Migration of Corneal Epithelial Cells during Wound Repair”. PloS one 8.8 (2013): e69642.

12 Zitationen in Europe PMC

Daten bereitgestellt von Europe PubMed Central.

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PMID: 29523772
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El Masri R, Seffouh A, Lortat-Jacob H, Vivès RR., Glycoconj J 34(3), 2017
PMID: 27812771
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The role of heparan sulphate in development: the ectodermal story.
Coulson-Thomas VJ., Int J Exp Pathol 97(3), 2016
PMID: 27385054
Sulfatase 2 facilitates lymphangiogenesis in breast cancer by regulating VEGF-D.
Zhu C, Qi X, Zhou X, Nie X, Gu Y., Oncol Rep 36(6), 2016
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Coulson-Thomas VJ, Chang SH, Yeh LK, Coulson-Thomas YM, Yamaguchi Y, Esko J, Liu CY, Kao W., Invest Ophthalmol Vis Sci 56(5), 2015
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Alcalde I, Íñigo-Portugués A, Carreño N, Riestra AC, Merayo-Lloves JM., Arch Soc Esp Oftalmol 90(10), 2015
PMID: 26101128
Quantitative stain-free and continuous multimodal monitoring of wound healing in vitro with digital holographic microscopy.
Bettenworth D, Lenz P, Krausewitz P, Brückner M, Ketelhut S, Domagk D, Kemper B., PLoS One 9(9), 2014
PMID: 25251440

76 References

Daten bereitgestellt von Europe PubMed Central.

Integrity of epithelium and endothelium in organ-cultured human corneas.
Crewe JM, Armitage WJ., Invest. Ophthalmol. Vis. Sci. 42(8), 2001
PMID: 11431439

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