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Originally published In Press as doi:10.1167/iovs.08-3359 on July 30, 2009
 (Investigative Ophthalmology and Visual Science. 2009;50:5690-5696.)
© 2009 by The Association for Research in Vision and Ophthalmology, Inc.
doi:10.1167/iovs.08-3359
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Detection of Differentially Expressed Wound-Healing–Related Glycogenes in Galectin-3–Deficient Mice

Chandrassegar Saravanan,1,2 Zhiyi Cao,1 Steven R. Head,3 and Noorjahan Panjwani1,2

From the 1Department of Ophthalmology and The New England Eye Center and the 2Program in Cell, Molecular and Developmental Biology, Tufts University School of Medicine, Boston, Massachusetts; and 3DNA Array Core Facility, The Scripps Research Institute, La Jolla, California.

Corresponding author: Noorjahan Panjwani, Department of Ophthalmology, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111; noorjahan.panjwani{at}tufts.edu.

Purpose. A prior study showed that exogenous galectin-3 (Gal-3) stimulates re-epithelialization of corneal wounds in wild-type (Gal-3+/+) mice but, surprisingly, not in galectin-3–deficient (Gal-3–/–) mice. In an effort to understand why the injured corneas of Gal-3–/– mice are unresponsive to exogenous Gal-3, the present study was designed to determine whether genes encoding the enzymes that regulate the synthesis of glycan ligands of Gal-3 are differentially expressed in Gal-3–/– corneas compared with the Gal-3+/+ corneas.

Methods. Glycogene microarray technology was used to identify differentially expressed glycosyltransferases in healing Gal-3+/+ and Gal-3–/– corneas.

Results. Of ~2000 glycogenes on the array, the expression of 8 was upregulated and that of 14 was downregulated more than 1.3-fold in healing Gal-3–/– corneas. A galactosyltransferase, β3GalT5, which has the ability to synthesize Gal-3 ligands was markedly downregulated in healing Gal-3–/– corneas. The genes for polypeptide galactosaminyltransferases (ppGalNAcT-3 and -7) that are known to initiate O-linked glycosylation and N-aspartyl-β-glucosaminidase, which participates in the removal of N-glycans, were found to be upregulated in healing Gal-3–/– corneas. Microarray data were validated by qRT-PCR.

Conclusions. Based on the known functions of the differentially expressed glycogenes, it appears that the glycan structures on glycoproteins and glycolipids, synthesized as a result of the differential glycogene expression pattern in healing Gal-3–/– corneas may lead to the downregulation of specific counterreceptors for Gal-3. This may explain, at least in part, why, unlike healing Gal-3+/+ corneas, the healing Gal-3–/– corneas are unresponsive to the stimulatory effect of exogenous Gal-3 on re-epithelialization of corneal wounds.






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