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Complementation of Splicing Activity by a Galectin-3 - U1 snRNP Complex on Beads
Published on: December 9, 2020
Perturbing O-GlcNAcase Modulates the Expression and Distribution of Galectin-3
Mana Mohan Mukherjee1, Asmita Pramanik2, Marcella Kolodrubetz1
1Cell Biochemistry Section, Laboratory of Cell and Molecular Biology, National Institute of Diabetes Digestive and Kidney Disease (NIDDK), National Institutes of Health, Bethesda, MD 20892, USA.
Cells
|July 13, 2026
Summary
The enzyme O-GlcNAcase (Oga) regulates Galectin-3 (Gal-3) levels. Oga deficiency reduces Gal-3, impacting its role in metabolic inflammation and biomarker interpretation.
Area of Science:
- Biochemistry and Molecular Biology
- Metabolic Disease Research
- Immunology
Background:
- Galectin-3 (Gal-3) is a lectin linked to metabolic inflammation, cardiovascular issues, and obesity.
- Understanding Gal-3's regulation is crucial, as it's a relevant biomarker for various diseases.
- O-GlcNAcase (Oga) is an enzyme involved in nutrient-sensitive signaling pathways relevant to Gal-3-associated diseases.
Purpose of the Study:
- To investigate the relationship between metabolic status and Galectin-3 (Gal-3) expression.
- To determine if O-GlcNAcase (Oga) regulates Gal-3 expression and systemic abundance.
Main Methods:
- Induction of obesity in male mice using a high-fat diet (HFD) for eight weeks.
- Measurement of serum and plasma Gal-3 concentrations via ELISA.
- Analysis of Gal-3 expression in Oga wild-type, heterozygous, and knockout mice using RT-qPCR.
Main Results:
- Obese mice exhibited significantly increased body weight, blood glucose levels, and circulating Gal-3 concentrations.
- Oga knockout mice showed significantly reduced circulating Gal-3 levels compared to wild-type and heterozygous mice.
- RT-qPCR confirmed genotype-dependent, tissue-specific regulation of Gal-3 mRNA expression by Oga.
Conclusions:
- O-GlcNAcase (Oga) is identified as a critical regulator of Galectin-3 (Gal-3) expression and systemic levels.
- A mechanistic link between Oga, O-GlcNAc signaling, and Gal-3-mediated metabolic inflammation is established.
- Oga activity influences Gal-3 homeostasis, potentially affecting its utility as a biomarker in metabolic diseases.
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