ArticleInvestigative ophthalmology & visual science2009
Detection of differentially expressed wound-healing-related glycogenes in galectin-3-deficient mice.
Article in Investigative ophthalmology & visual science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Galectin-3, a damage-associated molecular pattern, in tears of patients with vernal keratoconjunctivitis.Japanese journal of ophthalmology · 2023Article
- Increased Expression of Galectin-3 in Skin Fibrosis: Evidence from In Vitro and In Vivo Studies.International journal of molecular sciences · 2022Article
- Human trophoblast requires galectin-3 for cell migration and invasion.Scientific reports · 2019Article
- Galectin-3: One Molecule for an Alphabet of Diseases, from A to Z.International journal of molecular sciences · 2018Review
- Galectin-3: A Positive Regulator of Leukocyte Recruitment in the Inflamed Microcirculation.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Matricellular proteins in the trabecular meshwork: review and update.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2014Review
- Comparative Analysis of Glycogene Expression in Different Mouse Tissues Using RNA-Seq Data.International journal of genomics · 2014Article
- A glycobiology review: carbohydrates, lectins and implications in cancer therapeutics.Acta histochemica · 2011Review
- Matrilysin-1 (MMP7) cleaves galectin-3 and inhibits wound healing in intestinal epithelial cells.Inflammatory bowel diseases · 2011Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
purposeA 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.
methodsGlycogene microarray technology was used to identify differentially expressed glycosyltransferases in healing Gal-3(+/+) and Gal-3(-/-) corneas.
resultsOf approximately 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, beta3GalT5, 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-beta-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.
conclusionsBased 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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