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Journal of Biomedicine and Biotechnology
Volume 2010 (2010), Article ID 854927, 9 pages
Research Article

The Lipid Moiety of Haemozoin (Malaria Pigment) and P. falciparum Parasitised Red Blood Cells Bind Synthetic and Native Endothelin-1

1Dipartimento di Sanità Pubblica-Microbiologia-Virologia, Università degli Studi di Milano, via Pascal 36, 20133 Milan, Italy
2Dipartimento di Scienze Molecolari Applicate ai Biosistemi (DISMAB), Università degli Studi di Milano, via Trentacoste 2, 20134 Milan, Italy
3ISTM, CNR, via Venezian 21, 20133 Milan, Italy
4Fondazione IRCCS, Istituto Nazionale dei Tumori, via Venezian 1, 20133 Milan, Italy
5UNICEF/UNDP/WB/WHO Special Programme for Research & Training in Tropical Diseases (TDR), Avenue Appia 20, 1211 Geneva 27, Switzerland

Received 3 August 2009; Revised 8 November 2009; Accepted 29 December 2009

Academic Editor: Abhay R. Satoskar

Copyright © 2010 Nicoletta Basilico et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Endothelin1 (ET-1) is a 21-amino acid peptide produced by the vascular endothelium under hypoxia, that acts locally as regulator of vascular tone and inflammation. The role of ET-1 in Plasmodium falciparum malaria is unknown, although tissue hypoxia is frequent as a result of the cytoadherence of parasitized red blood cell (pRBC) to the microvasculature. Here, we show that both synthetic and endothelial-derived ET-1 are removed by parasitized RBC (D10 and W2 strains, chloroquine sensitive, and resistant, resp.) and native haemozoin (HZ, malaria pigment), but not by normal RBC, delipidized HZ, or synthetic beta-haematin (BH). The effect is dose dependent, selective for ET-1, but not for its precursor, big ET-1, and not due to the proteolysis of ET-1. The results indicate that ET-1 binds to the lipids moiety of HZ and membranes of infected RBCs. These findings may help understanding the consequences of parasite sequestration in severe malaria.