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PMID:27058125
| Citation |
DeSantis-Rodrigues, A, Chang, YC, A Hahn, R, P Po, I, Zhou, P, Lacey, CJ, Pillai, A, C Young, S, A Flowers Ii, R, A Gallo, M, D Laskin, J, R Gerecke, D, K H Svoboda, K, D Heindel, N and Gordon, MK (2016) ADAM17 Inhibitors Attenuate Corneal Epithelial Detachment Induced by Mustard Exposure. Invest. Ophthalmol. Vis. Sci. 57:1687-1698 |
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| Abstract |
Sulfur mustard, nitrogen mustard (NM), and 2-chloroethyl ethyl sulfide all cause corneal injury with epithelial-stromal separation, differing only by degree. Injury can resolve in a few weeks or develop into chronic corneal problems. These vesicants induce microbullae at the epithelial-stromal junction, which is partially caused by cleavage of transmembranous hemidesmosomal collagen XVII, a component anchoring the epithelium to the stroma. ADAM17 is an enzyme involved in wound healing and is able to cleave collagen XVII. The activity of ADAM17 was inhibited in vesicant-exposed corneas by four different hydroxamates, to evaluate their therapeutic potential when applied 2 hours after exposure, thereby allowing ADAM17 to perform its early steps in wound healing. |
| Links |
PubMed Online version:10.1167/iovs.15-17269 |
| Keywords |
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Significance
Annotations
| Gene product | Qualifier | GO Term | Evidence Code | with/from | Aspect | Extension | Notes | Status |
|---|---|---|---|---|---|---|---|---|
| GO:0019838: growth factor binding |
ECO:0000315: |
F |
seeded from uniprot |
complete | ||||
| GO:0061581: corneal epithelial cell migration |
ECO:0000314: |
P |
Figure 3. shows the ADAM17 activity in unexposed and NM-exposed corneas. Figure 4.B shows the immunofluorescence of corneas using an anti-human ADAM17 ectodomain antibody. This visualizes active ADAM17 immunoreactivity. |
complete | ||||
Notes
See also
References
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