Naslov
Galectin-3 Role and Trafficking in Different Macrophage Phenotypes

Autori
Lepur, Adriana ; Carlsson, Michael C. ; Salomonsson, Emma ; Dumić, Jerka ; Leffler, Hakon

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
HDBMB 2010 "The secret life of biomolecules" ; Book of Abstracts / Kovarik, Zrinka ; Varljen, Jadranka - Rijeka : Hrvatsko društvo za biokemiju i molekularnu biologiju (HDBMB), 2010, SYM-SP2/P42

Skup
10th Congress of the Croatian Society of Biochemistry and Molecular Biology, The Secret Life of Biomolecules

Mjesto i datum
Opatija, Hrvatska, 15.09.2010. - 18.09.2010

Vrsta sudjelovanja
Poster

Vrsta recenzije
Domaća recenzija

Ključne riječi
macrophages; galectin-3; trafficking

Sažetak
Classically and alternatively activated macrophages were established by differently treating the THP-1 monocyte cell line. PMA treatment of THP-1 monocytes results in their differentiation into macrophages. After subsequent LPS treatment, macrophages gave rise to an M1 phenotype and after IL-4+PMA a phenotype we named M2. Here we confirm that M1 macrophages release higher amounts of inflammatory cytokines compared to M2 or untreated macrophages. It has been reported that galectin-3, a β-galactoside binding lectin is crucial for M2 macrophages development. As well, we demonstrate different patterns of galectin-3 expression in different macrophages. Macrophages can also excrete produced galectin-3. Extracellular galectin-3 can then act on the surrounding cells or be taken back by the macrophages. Hence, endocytosis of galectin-3 and its R186S mutant was inspected. The R186S mutant was made by point mutation in carbohydrate recognition domain (CRD) of galectin-3, resulting in diminished β-galactoside binding activity. Although β-galactoside binding was thought to be essential for galectin-3 endocytosis, we found that macrophages can uptake the R186S mutant, too. Galetin-3 and the R186S mutant take different routes when entering the macrophages and the mechanism of endocytosis seams to differ depending on the macrophage phenotype. Different macrophages, especially M2 macrophages can be found in asthmatic lungs. To examine their influence on lung fibroblasts, supernatants of differently treated THP-1 cells were collected and added to the HFL-1 fibroblast cell line. M2 macrophages supernatant promoted HFL-1 cells fibroblastic activity, illustrated by size and sprouting seen after actin immuno-stain of the cells, compared to the effect of other macrophages supernatants. Finding a way to modulate or stop the development of certain macrophage phenotypes, e.g. by using galectin inhibitors, could mean easing a vast palette of pathological conditions.

Izvorni jezik
Engleski

Znanstvena područja
Biologija

POVEZANOST RADA