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Glycobiology Advance Access originally published online on February 3, 2006
Glycobiology 2006 16(5):359-367; doi:10.1093/glycob/cwj085
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© The Author 2006. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Hyaluronan oligosaccharides induce cell death through PI3-K/Akt pathway independently of NF-{kappa}B transcription factor

Laura Alaniz1,2,*, Mariana G. García2,{dagger}, Carola Gallo-Rodriguez3,{ddagger}, Rosalía Agusti3, Norma Sterín-Speziale4,{ddagger}, Silvia E. Hajos2,{ddagger},§ and Elida Alvarez2,{ddagger},§

2 Cátedra de Inmunología-IDEHU, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, UBA- CONICET, Buenos Aires, Argentina; 3 Departamento de Química Orgánica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires (UBA), CIHIDECAR-CONICET, Buenos Aires, Argentina; and 4 Departamento de Ciencias Biológicas, Facultad de Farmacia y Bioquímica, UBA, IQUIFIB-CONICET, Buenos Aires, Argentina

1 To whom correspondence should be addressed; e-mail: laualaniz{at}ffyb.uba.ar

Received on July 1, 2005; revised on January 23, 2006; accepted on January 28, 2006

Several studies indicate that hyaluronan oligosaccharides (oHA) are able to modulate growth and cell survival in solid tumors; however, no studies have been undertaken to analyze the effect of oHA on T-lymphoid disorders. In this work we showed that oHA were able to induce apoptosis in lymphoma cell lines. Since PI3-K/Akt and nuclear factor-{kappa}B (NF-{kappa}B) are major factors involved in cell survival and anti-apoptotic pathways in lymphoma cells, we hypothesized that oHA could induce apoptosis through inhibition of these pathways. oHA were identified by a method which allows characterization of length using a high pH anion exchange chromatography with pulse amperometric detection (HPAEC-PAD). oHA inhibited PIP3 production (principal product of PI3-K activity) and reduced Akt phosphorylation levels, similarly to the specific inhibitor wortmannin. However, treatment with either oHA or wortmannin failed to inhibit constitutive NF-{kappa}B activity and modulate I{kappa}B{alpha} protein levels, suggesting that PI3-K and NF-{kappa}B signaling pathways are not related in the cell lines used. Cell behavior differed using native hyaluronan (HA), which induced PIP3 production, Akt phosphorylation, and NF-{kappa}B activation, although not related with cell survival since treatment with native HA showed no effect on apoptosis. Our results suggest that oHA induce apoptosis by suppression of PI3-K/Akt cell survival pathway without involving NF-{kappa}B activation, through a mechanism that differs from the one mediated by native HA.

Key words: apoptosis / HPAEC-PAD / hyaluronan oligomers / NF-{kappa}B / PI3-K / Akt

* Fellow from CONICET.

{dagger} Fellow from UBA.

{ddagger} Members of the National Research Career (CONICET).

§ These authors contributed equally to this work.


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