Naslov
Induction of galectin-3 by uv-light is mediated by both AP-1 and NF-kappaB signaling pathways
(Induction of galectin-3 by UV-light is mediated by both AP-1 and NF-kappaB signaling pathways)

Autori
Dumić, Jerka

Vrsta, podvrsta i kategorija rada
Radovi u zbornicima skupova, cjeloviti rad (in extenso), znanstveni

Izvornik
Italian Biochemical Society Transaction Vol. 15 / D'Alessio i sur. - Napulj : Societa Italiana di Biochimica e Biologia Molecolare, 2000, 237-237

Skup
Societa Italiana di Biochimica e Biologia Molecolare 45 Congresso Nazionale

Mjesto i datum
Napulj, Italija, 20.09.2000. - 23.09.2000

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
galectin-3; UV light; AP-1; NF-kappaB

Sažetak
INTRODUCTION: Galectin-3 is a ť32 kDa lectin that specifically binds to b-galactose on the non-reducing termini of oligosaccharide structures. Though it was first described as a macrophage surface antigen (1), subsequently it was shown to be involved in many different biological processes, including growth regulation (2), cell differentiation (3), adhesion (4), neoplastic transformation and tumor metastasis (5). One of the early studies suggested that galectin-3 might be involved in the heat-shock response [9], but very little is known about the expression of galectin-3 in stress. Aiming to learn more about the role of galectin-3 in the adaptation of cells to hostile environment, we have analyzed expression of galectin-3 in cells exposed to UV-C radiation. MATERIALS AND METHODS: Protein levels of galectin-3 were measured by western-blot analysis using M3/38 monoclonal antibody. To study effects of UV-C light, glioblastoma cells were irradiated by Phillips UVT 15W/G15T T8 lamp with emission maximum at 254 nm. The intensity of irradiation was determined using BioBlock VLX-3W dosimeter. Cells were grown in tissue culture dishes (60 ´ 15 mm), and the culture medium was briefly removed for the exposure. After the calculated exposure time (10 – 20 s depending on the irradiation dose), cells were supplemented with fresh medium and returned to the incubator. The involvement of transcription factors NF-kB and Jun in the induction of galectin-3 was addressed using specific inhibitor of NF-kB (zL3-vs) and antisense-jun oligonucleotides. RESULTS: We found that exposure to UV-C light (λ=254 nm, 40 and 80 J/m2) nearly doubles the expression of galectin-3 within one hour after the exposure and galectin-3 remains at the approximately same level for the next 24 h. Based on the published structure of the promotor region of human galectin-3 gene (LGALS3) and roles of AP-1 and NF-kB in the stress response, we speculated that these two transcription factors might also have a role in the regulation of galectin-3 expression after exposure to UV-C irradiation. To test this hypothesis we have used antisense-jun oligonucleotides and zL3-vs, a specific proteasome inhibitor that prevents degradation of IkB, and blocks transcriptional activation through NF-kB. Treatment of cells with antisense-jun oligonucleotides caused slow, but statistically significant and continuos decrease in galectin-3. After 10 h of cultivation in the presence of antisense-jun, the level of galectin-3 was about 60% of the initial value. At the same time, in cells that were treated with nonsense-jun oligonucleotides, levels of galectin-3 did not change, suggesting that Jun is involved in the regulation of the basal level of galectin-3 expression. However, even when the expression of Jun was significantly attenuated by antisense-jun oligonucleotides, UV-C irradiation still caused some increase in galectin-3 and moreover, this increase started within minutes after the exposure, when it is to early to see effects of newly-synthesized Jun. To check whether NF-kB is involved in the induction of galectin-3 by UV-C light, we have used zL3-vs to block transcriptional activation through NF-kB. Treatment of cells with zL3-vs did not have any effect on the basal level of galectin-3 in the first 4 h of incubation. However, when cells pre-treated with zL3-vs were exposed to UV-C radiation, the increase of galectin-3 that was visible in the control cells, was nearly completely absent. Thus the early phase of induction of galectin-3 following the exposure to UV-C radiation seems to be mediated by NF-kB. 1. Ho MK et al. (1982) J. Immunol. 128:1221-1228. 2. Moutsatsos IK et al. (1987) Proc. Natl. Acad. Sci. USA 84:6452-6456. 3. Bao Q et al. (1999) Glycobiology 9:489-495. 4. Inohara H et al. (1995) Cancer Res. 55:3267-3271. 5. Raz A et al. (1986) Cancer Res 46:3667-3672. 6 Sato S et al. (1993) Exp. Cell Res. 207:8-18.

Izvorni jezik
Engleski

Znanstvena područja
Biologija

POVEZANOST RADA