engleski

Modulation of galectin-3 expression by anti-inflammatory drugs

During the last few decades, the effects of anti-inflammatory drugs on numerous molecules and biological processes have been widely studied. Nevertheless, the relationship between anti-inflammatory drugs and lectin's expression/function is still to be elucidated. Galectin-3, a β -galactoside binding lectin, was found to be involved in regulation of numerous cellular functions ; intracellularly, it modulates cell growth, apoptosis and cell cycle while extracellularly, through the binding of various membrane receptors as well as extracellular matrix proteins, it regulates cell activation or apoptosis, modulates cell adhesion and induces cell migration. Since galectin-3 in general acts as a strong pro-inflammatory signal we have explored the effects of various anti-inflammatory drugs on galectin-3 expression. The results showed that anti-inflammatory drugs applied in clinically relevant doses affect both gene (LGALS3) and protein expression level of galectin-3. The provoked changes on protein level are qualitatively and quantitatively different comparing to the effects on galectin-3 mRNA level, indicating that galectin-3 expression is regulated both transcriptionally and post-transcriptionally. We also observed that the effects of anti-inflammatory on galectin-3 expression depend on the activation state of the cell, drug type and applied concentration as well as time of the exposure demonstrating that the regulation of galectin-3 expression is a complex, fine-tuned mechanism that involves numerous transcription factors and signaling pathways. Our data revealed galectin-3 as a new target molecule of anti-inflammatory drugs, contributing to the better understanding of physiological role of galectin-3 and expanding the knowledge about the mechanisms of action of immunomodulatory drugs needed for development of new therapeutical procedures.

galectin-3; anti-inflammatory drugs

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