Abstract
Previous studies on endogenous galectin-3 proved its role in the pathogenesis of asthma, heart attack and obesity. Galectin-3 applied therapeutically as gene therapy suppresses the inflammatory response in a rat asthma model thus presenting novel therapeutic approach to the treatment of several diseases. Despite availability of enormous data concerning galectin-3 expression, the mechanisms of regulation of galectin-3 expression are relatively poorly defined. Galectins are either pro-inflammatory or anti-inflammatory, such as galectin-1, may be employed as anti-inflammatory agents, while others, such as galectin-3, are evidently suitable targets for anti-inflammatory drugs. Investigating galectin-3 in the immune response has demonstrated that this protein displays pro- and anti-inflammatory roles depending on the target cell type, whether galectin-3 is acting exogenously or endogenously, its expression level and other inflammatory factors. It is therefore imperative that all these factors be taken into consideration should galectin-3 be used therapeutically.
Highlights
Previous studies on endogenous galectin-3 proved its role in the pathogenesis of asthma, heart attack and obesity
Investigating galectin-3 in the immune response has demonstrated that this protein displays pro- and anti-inflammatory roles depending on the target cell type, whether galectin-3 is acting exogenously or endogenously, its expression level and other inflammatory factors
The presence of cAMP-dependent response elements (CRE) and NF-κB-like sites in the promoter region suggests that galectin-3 expression could be regulated through metabolic/signaling pathways involving the cAMP-response element-binding protein (CREB) or the NF-κB transcription factor that is at the core of inflammatory pathways[6]
Summary
Previous studies on endogenous galectin-3 proved its role in the pathogenesis of asthma, heart attack and obesity. Investigating galectin-3 in the immune response has demonstrated that this protein displays pro- and anti-inflammatory roles depending on the target cell type, whether galectin-3 is acting exogenously or endogenously, its expression level and other inflammatory factors. In addition to five putative Sp1 binding sites, the promoter region of the human LGALS3 gene contains 5 cAMP-dependent response elements (CRE), 4 AP-1 transcription factor binding sites and 1 AP-4-like consensus sequence, two NFκB-like motifs, sis-inducible element (SIE) and a consensus basic helix-loop-helix (bHLH) core sequence[3,4,5].
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